New Type of Age-Related Memory Loss Identified – Neuroscience News

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Summary: Researchers established new criteria for Limbic-predominant Amnestic Neurodegenerative Syndrome (LANS), a memory-loss condition often mistaken for Alzheimers disease.

Unlike Alzheimers, LANS progresses more slowly and has a better prognosis. The criteria help doctors diagnose LANS in living patients using brain scans and biomarkers. This advancement aids in better management and tailored treatments for memory loss.

Key Facts:

Source: Mayo Clinic

Researchers atMayo Clinichave established new criteria for a memory-loss syndrome in older adults that specifically impacts the brains limbic system. It can often be mistaken for Alzheimers disease.

The good news: Limbic-predominant Amnestic Neurodegenerative Syndrome, or LANS, progresses more slowly and has a better prognosis, and is now more clearly defined for doctors working to find answers for memory loss patients.

Prior to the researchers developing clinical criteria published in the journalBrain Communications, the hallmarks of the syndrome could be confirmed only by examining brain tissue after a persons death.

The proposed criteria provide a framework for neurologists and other experts to classify the condition in patients living with symptoms, offering a more precise diagnosis and potential treatments. They consider factors such as age, severity of memory impairment, brain scans, and biomarkers indicating the deposits of specific proteins in the brain.

The criteria were developed and validated using data from more than 200 participants in databases for theMayo Clinic Alzheimers Disease Research Center, theMayo Clinic Study of Agingand the Alzheimers Disease Neuroimaging Initiative.

Understanding the condition will lead to better management of symptoms and more tailored therapies for patients suffering from this type of cognitive decline, distinct from Alzheimers disease, saysDavid T. Jones, M.D., a Mayo Clinic neurologist and senior author of the study.

In our clinical work, we see patients whose memory symptoms appear to mimic Alzheimers disease, but when you look at their brain imaging or biomarkers, its clear they dont have Alzheimers. Until now, there has not been a specific medical diagnosis to point to, but now we can offer them some answers, Jones says.

This research creates a precise framework that other medical professionals can use to care for their patients. It has major implications for treatment decisions, including amyloid-lowering drugs and new clinical trials, and counseling on their prognosis, genetics and other factors.

Decades of work to understand and classify different types of dementia is ongoing, says Nick Corriveau-Lecavalier, Ph.D., the papers first author. These findings build upon scientists continued efforts to untangle neurological conditions that often have similar symptoms or can occur simultaneously, but can have drastically different treatments and prognoses.

Historically, you might see someone in their 80s with memory problems and think they may have Alzheimers disease, and that is often how its being thought of today, Corriveau-Lecavalier says.

With this paper, we are describing a different syndrome that happens much later in life. Often, the symptoms are restricted to memory and will not progress to impact other cognitive domains, so the prognosis is better than with Alzheimers disease.

Without signs of Alzheimers disease, the researchers looked at the involvement of one possible culprit a buildup of a protein called TDP-43 in the limbic system that scientists have found in the autopsied brain tissue of older adults.

Researchers have classified the build-up of these protein deposits aslimbic-predominant age-related TDP-43 encephalopathy, or LATE. These protein deposits could be associated with the newly defined memory loss syndrome, but there are also other likely causes and more research is needed, the authors say.

With clinical criteria established by Jones, Corriveau-Lecavalier and co-authors, practitioners could soon diagnose LANS in patients so those living with memory loss might better understand options for treatment and potential progression of the disease, opening doors for research to further illuminate the characteristics of the disease.

Funding: The research was funded in part by National Institutes of Health grants P30 AG062677, P50 AG016574, U01 AG006786, R37 AG011378 and R01 AG041851 and by the Robert Wood Johnson Foundation, the Elsie and Marvin Dekelboum Family Foundation, the Liston Family Foundation, the Edson Family, the Gerald A. and Henrietta Rauenhorst Foundation and the Foundation Dr. Corinne Schuler.

Drs. Jones and Corriveau-Lecavalier reported no conflicts of interest. A complete list of co-authors and financial disclosures is available in the manuscript.

Author: Emily DeBoom Source: Mayo Clinic Contact: Emily DeBoom Mayo Clinic Image: The image is credited to Neuroscience News

Original Research: Open access. Clinical criteria for a limbic-predominant amnestic neurodegenerative syndrome by David T. Jones et al. Brain Communications

Abstract

Clinical criteria for a limbic-predominant amnestic neurodegenerative syndrome

Predominant limbic degeneration has been associated with various underlying aetiologies and an older age, predominant impairment of episodic memory and slow clinical progression. However, the neurological syndrome associated with predominant limbic degeneration is not defined.

This endeavour is critical to distinguish such a syndrome from those originating from neocortical degeneration, which may differ in underlying aetiology, disease course and therapeutic needs.

We propose a set of clinical criteria for a limbic-predominant amnestic neurodegenerative syndrome that is highly associated with limbic-predominant age-related TDP-43 encephalopathy but also other pathologic entities.

The criteria incorporate core, standard and advanced features, including older age at evaluation, mild clinical syndrome, disproportionate hippocampal atrophy, impaired semantic memory, limbic hypometabolism, absence of neocortical degeneration and low likelihood of neocortical tau, with degrees of certainty (highest, high, moderate and low).

We operationalized this set of criteria using clinical, imaging and biomarker data to validate its associations with clinical and pathologic outcomes.

We screened autopsied patients from Mayo Clinic and Alzheimers Disease Neuroimaging Initiative cohorts and applied the criteria to those with an antemortem predominant amnestic syndrome (Mayo,n= 165; Alzheimers Disease Neuroimaging Initiative,n= 53) and who had Alzheimers disease neuropathological change, limbic-predominant age-related TDP-43 encephalopathy or both pathologies at autopsy.

These neuropathology-defined groups accounted for 35, 37 and 4% of cases in the Mayo cohort, respectively, and 30, 22 and 9% of cases in the Alzheimers Disease Neuroimaging Initiative cohort, respectively.

The criteria effectively categorized these cases, with Alzheimers disease having the lowest likelihoods, limbic-predominant age-related TDP-43 encephalopathy patients having the highest likelihoods and patients with both pathologies having intermediate likelihoods.

A logistic regression using the criteria features as predictors of TDP-43 achieved a balanced accuracy of 74.6% in the Mayo cohort, and out-of-sample predictions in an external cohort achieved a balanced accuracy of 73.3%. Patients with high likelihoods had a milder and slower clinical course and more severe temporo-limbic degeneration compared to those with low likelihoods. S

tratifying patients with both Alzheimers disease neuropathological change and limbic-predominant age-related TDP-43 encephalopathy from the Mayo cohort according to their likelihoods revealed that those with higher likelihoods had more temporo-limbic degeneration and a slower rate of decline and those with lower likelihoods had more lateral temporo-parietal degeneration and a faster rate of decline.

The implementation of criteria for a limbic-predominant amnestic neurodegenerative syndrome has implications to disambiguate the different aetiologies of progressive amnestic presentations in older age and guide diagnosis, prognosis, treatment and clinical trials.

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New Type of Age-Related Memory Loss Identified - Neuroscience News

Neurology ‘House Calls’ to Improve Quality of Care and Life for ALS Patients – Mega Doctor News

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Dr. Keelie Denson, a second-year neurology resident at Houston Methodist, watched first-hand as her father James and family faced ALS from her childhood until his death when she was 13. Image of illustration purposes

Mega Doctor News

ByPattiMuckHouston Methodist

Newswise Robert Amar, a U.S. Army veteran, was diagnosed with Amyotrophic Lateral Sclerosis when he was a fit and healthy 45 years old. Fourteen years later, he has lost his ability to walk, talk, swallow and breathe on his own.

His high school sweetheart Angela, and the couples three adult children Victoria, Robert and Marissa and a few dedicated caregivers are his 24/7 caretakers. Commonly known as Lou Gehrigs disease after the New York Yankees hero of the 1930s, ALS is an incurable disease of the neuromuscular system. The diseases progression and symptoms vary widely from patient to patient, ultimately giving the patient a ringside seat as their bodies melt away, says Dr. Stanley Appel, director of the Johnson Center for Cellular Therapeutics at Houston Methodist and internationally respected ALS expert. He founded the nations first multidisciplinary ALS Clinic at Houston Methodist in 1982.

You hear those three letters A-L-S and it just changes your whole life forever, says Angela, Roberts wife of 29 years. We just love him so much and we would do anything for him.

Robert is among the first Houston Methodist ALS patients enrolled in a research study designed to provide a multidisciplinary standard of care to those whose disease has rendered them homebound.

24 ALS patients enrolled in first-of-its-kind study

Dr. Keelie Denson, a second-year neurology resident at Houston Methodist, watched first-hand as her father James and family faced ALS from her childhood until his death when she was 13. As patients progress in their disease, it becomes harder and harder for them to make it to multidisciplinary care visits in a clinic setting, says Dr. Denson. These are already geographically sparse to begin with.

Eventually, ALS patients and their families can be overwhelmed by the struggle to obtain consistent continuity of care from their team of specialists neurologists, social workers, speech therapists, physical and occupational therapists and dietitians. Worst case scenario? They stop attending clinic and drop off physicians radar.

Were being pulled out at the stage of the disease where our patients are most vulnerable and need us most, says Dr. Denson. There are no studies or resulting data to address this critical need. Until now.

Supported by Dr. Ericka Greene and the multidisciplinary ALS team at Houston Methodist, Dr. Denson designed a study, Caring for the Homebound Patient with ALS, that is following 24 patients and an optional 24 caregivers for 16 months. Patients live within 50 miles of Houston and cant physically visit their neurology team any longer, maybe because theyre too weak and on a ventilator or they dont have transportation, lack access to technology or have financial hardship. For one reason or another, theyve missed one or more clinic visits and are basically on their own in the final stages of their disease.

Half the patients the control group will receive telehealth visits with a neurologist. The other half the intervention group will get quarterly home visits from a neurologist and a social worker, accompanied by a live video conference that includes physical and occupational therapists, a dietitian, a speech therapist, and a medical equipment expert.

Before each visit and at the end of the study, patients and caregivers will complete the gold standard quality of life surveys that will provide data to prove or disprove the theory that multidisciplinary home health care visits improve life for these ALS patients.

If this program meets its endpoints and proves to be feasible, there will be an opportunity to create guidelines and curriculum for other institutions to replicate the program across the nation, Dr. Denson says. Our hope is that this program will become a covered health care service for patients who are homebound because of ALS.

Back to the Basics

Early in the study planning stage, Dr. Denson questioned her ALS families about what they found lacking in ALS care. For the Amar family, the answer was easy: Hands-on care for our loved ones, Angela recalls. As her husbands disease progressed, getting him to the ALS Clinic and other appointments became a monumental struggle. For Robert, leaving home was becoming impossible. It is also very difficult to find caregivers and nurses experienced in caring for someone on a ventilator, feeding tube dependent, non-verbal and paralyzed.

Still, the close-knit family counted their blessings. They were able to celebrate milestones that many ALS families never get to see. Robert met his goal of watching all three children graduate from high school, and then from Texas A&M University. His oldest daughter Victoria hopped on his lap and they did an impromptu wheelchair dance at her wedding. Recently, the first and only grandson Gavin attended his first Houston Astros game at Minute Maid Park and brought his grandfather an Astros T-shirt to Houston Methodist Hospital where Robert was recovering from a recent tracheostomy surgery. A season ticketholder before ALS entered his life, Robert and his family attended Astros World Series games twice. He always made it a point to cheer on his favorite team.

Robert has always been very determined, and he has this positive attitude that Im going to live each day like I always have to the fullest. Angela says.

On the day of his first home visit, Robert was cleaned up, comfortable in his bed, happy and ready to see his team. Five minutes later, complications with his new tracheostomy for breathing, combined with the movement of the morning routine, sent his oxygen levels plummeting. Things can change in a heartbeat, Angela says. Im usually very strong, but I did break down a little bit. It was a very bad day for Robert, but the team got to see the good and the bad. Youre sharing your life with them, and you can see in their faces how concerned they are and how much they care.

Dr. Densons presentation of the ALS home care study generated considerable enthusiasm at an ALS symposium in Switzerland last year, and results will be compiled into a formal report following the 16-month trial.

For more information on Houston Methodists ALS Clinic, visitwww.houstonmethodist.org/ALS-Clinic

This study is possible because of support from The Constance M. and Byron F. Dyer Fellowship and The Lou and Eleanor Gehrig Family Foundation.

Postscript:Robert Amar passed away shortly after his 59thbirthday in mid-May 2024. His life of courage and determination lives on in Kingwood High Schools annual Robert Amar Mental Toughness Award and in his participation in Caring for the Homebound Patient with ALS, the research program outlined in this story designed to help ALS patients now and in the future.

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Inherited Alzheimer’s: Whether It’s From Mom or Dad Could Matter – HealthDay

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MONDAY, June 17, 2024 (HealthDay News) -- Genetics can play a role in a person's odds for Alzheimer's disease, and new research suggests differences in that risk are based on which parent had the illness.

In a study of 4,400 people still "cognitively unimpaired," there was higher buildup of amyloid protein plaques in the brain (a hallmark of Alzheimer's) if either the person's mother, or both parents, had Alzheimer's, compared to folks where Alzheimer's had only struck the father.

People with an Alzheimer's-affected mother may therefore be at special risk, said a team from Mass General Brigham, in Boston.

"Maternal inheritance of Alzheimers disease may be an important factor in identifying asymptomatic individuals for ongoing and future prevention trials, said study co-author Dr Reisa Sperling, a neurologist at Mass General.

The findings were published June 17 in the journal JAMA Neurology.

The study was based on data from a clinical trial focused on Alzheimer's prevention. People in the study were asked about whether or not either of their parents had ever been diagnosed with Alzheimer's disease, and when their parent's memory began to fail.

Sperling and colleagues then compared those answers to levels of amyloid in people's brains.

Having had a father who developed Alzheimer's symptoms relatively late in life did not seem to be related to levels of amyloid in people's brains, the research showed.

However, there was a correlation between the accumulation of brain plaques and having had a mother whose Alzheimer's symptoms began at any age, or having a father whose symptoms began relatively early, the team reported.

If your father had early-onset symptoms, that is associated with elevated [amyloid] levels in the offspring, said study first author Dr. Mabel Seto, a postdoctoral research fellow in the hospital's department of neurology. However, it doesnt matter when your mother started developing symptoms -- if she did at all, its associated with elevated amyloid.

The sex of the study participant did not seem to matter when it came to the relationship between amyloid buildup and parental histories, the researchers noted.

Its also important to note a majority of these participants are non-Hispanic white, Seto added in a Brigham news release. We might not see the same effect in other races and ethnicities.

More information

Find out more about Alzheimer's disease and genetics at the Alzheimer's Association.

SOURCE: Mass General Brigham, news release, June 15, 2024

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Ascidian Therapeutics Enters Collaboration with Roche for Discovery and Development of RNA Exon Editing … – PR Newswire

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Ascidian to receive $42 million in initial payment, and up to $1.8 billion in research, clinical and commercial milestone payments, as well as commercial royalties

Per-target agreement enables Ascidian to pursue additional internal and collaborative programs within neurology and other therapeutic areas

Combines RNA Exon Editors with next generation CNS delivery capabilities of Roche to develop novel medicines for difficult to treat neurological diseases

BOSTON, June 18, 2024 /PRNewswire/ --Ascidian Therapeutics, a biotechnology company seeking to treat human diseases by rewriting RNA, today announced a research collaboration and licensing agreement with Roche (SIX: RO, ROG;OTCQX: RHHBY) for the discovery and development of RNA exon editing therapeutics targeting neurological diseases.

Ascidian's RNA exon editing platform is designed to advance the therapeutic possibilities of RNA medicine and treat diseases not addressed by today's gene editing technologies. The company designs and develops RNA exon editing therapeutics that edit RNA exons at the kilobase scale.

Under the agreement, Ascidian will provide Roche exclusive, target-specific rights to Ascidian's RNA exon editing technology for undisclosed neurological targets. Ascidian will conduct discovery and certain preclinical activities in collaboration with Roche, and Roche will be responsible for certain preclinical activities, and further clinical development, manufacturing, and commercialization. Ascidian will receive an initial payment of $42 million and is eligible to receive up to $1.8 billion in research, clinical, and commercial milestone payments, as well as royalties on commercial sales worldwide. Based on the terms of the agreement, Ascidian is free to develop programs against other neurological targets internally or with other collaborators.

"Roche is known and respected worldwide for their expertise in complex neurological diseases, and I am proud of the scientific rigor and quality of the work done at Ascidian that has led to this partnership," saidMichael Ehlers,M.D., Ph.D., President and Chief Executive Officer of Ascidian Therapeutics. "The potential of treating disease by large-scale exon editing of RNA is vast. We look forward to working with the Roche team to develop first-in-class RNA exon editing medicines for multiple neurological diseases, with a mission and passion to relieve suffering and improve lives."

"Our partnership with Ascidian is an opportunity to harness advanced RNA exon editing technology, which has the potential to deliver transformative one-time therapeutics by editing multiple whole exons at the RNA level with a single treatment," said James Sabry, M.D., Ph.D., Global Head of Pharma Partnering at Roche.

Ascidian's platform enables targeting of large genes and genes with high mutational variance while maintaining native gene expression patterns and levels. By rewriting RNA, Ascidian's exon editing technology is designed to provide the durability of gene therapy, while sharply reducing risks associated with direct DNA editing and gene replacement.

About Ascidian Therapeutics

Ascidian Therapeutics, an ATP company, is redefining the treatment of disease by rewriting RNA. By editing exons at the RNA level, Ascidian therapies enable precise post-transcriptional editing of genes, resulting in full-length, functional proteins at the right levels, in the right cells, at the right time. With discovery, preclinical, and clinical programs in retinal, neurological, neuromuscular, and genetically defined diseases, Ascidian's approach has the potential to treat patients with one dose of an RNA exon editor, opening new therapeutic possibilities for patients and their families who are seeking breakthroughs. Earlier this year, Ascidian announced U.S. FDA IND clearance for the first-ever RNA exon editing candidate, ACDN-01, which targets Stargardt disease and other ABCA4 retinopathies. Ascidian is currently executing the Phase 1/2 STELLAR clinical trial to evaluate the safety and efficacy of ACDN-01. For more information, visit http://www.ascidian.com.

SOURCE Ascidian Therapeutics

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Ascidian Therapeutics Enters Collaboration with Roche for Discovery and Development of RNA Exon Editing ... - PR Newswire

Neurology residents offering virtual field trip into the brain – University of Nebraska Medical Center

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A group of UNMC neurology residents are offering Nebraska students a field trip into the human brain.

For the Nebraska 4-H programs virtual field trips series, residents Isha Snehal, MBBS, Kanchan Kumari, MD, and Zaid Najdawi, MD, worked with the University of Nebraska-Lincolns Nebraska Extension to create a video on brain issues around epilepsy, stroke and concussions.

The series is geared toward Nebraska high school students and originally was established during the pandemic to offer engaging virtual experiences in STEM and ag-related fields, said Sarah Paisley, an associate educator with Nebraska Extension based out of Garden and Morrill Counties.

The program reached out to the UNMC Department of Neurological Sciences, hoping to show the complexity of the brain and what happens after a trauma.

Click Play below to see the video titled, Neurology Whats Going on with My Brain?

Dr. Snehal said awareness of strokes, epilepsy and concussions is important because of the large number of people they affect. Not only have many high school students heard or experienced those issues in different ways, they also could learn how to help if those problems happen around them, she said.

The hope is that the outreach can educate and create awareness about these issues among as many kids as possible, Dr. Snehal said, and they can use some of the tips when they do find themselves in a situation to help others.

Paisley said the video also highlights some great neurological studies going on right here in Nebraska at UNMC.

If students are interested in health care as a career, it allows them to explore an area they could pursue, Paisley said. If it wasnt an area of interest before, she said, the field trip exposes them to UNMC and neurology for the future.

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Neurology residents offering virtual field trip into the brain - University of Nebraska Medical Center

A neurologist took DIY treatments seriously. Has it sparked a breakthrough? – WHYY

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Vitamins, unapproved serums in glass vials, even acupuncture programs. His patients slowly opened up to Bedlack about dozens of supposedly effective elixirs and therapies touted on sketchy websites or anonymous forums that they were trying. The kind of treatments that were easy for physicians to dismiss or ignore.

Really they werent even being recorded, much less talked about like they werent getting into any medical records at the time, said Bedlack. When people were checking in, nurses were only interested in medicines. They werent interested in vitamins and supplements and products that maybe couldnt even be characterized. So, one day I asked, What is all this stuff? and somebody said, well, I figured you probably wouldnt want to talk about this. And then, the more I thought about it, I said, Wow, if this is a common thing that people are doing this, shouldnt I be interested?

His patients simply didnt have time to wait on the conclusions of lengthy clinical trials that might never come for these products and programs. If they were looking elsewhere for answers, Bedlack felt he had a responsibility to weigh in on what they were trying rather than dismiss it all off-hand.

Shouldnt I want to partner with patients using my years of training to try to help them make more informed decisions about these? said Bedlack.

Many of his colleagues in medicine disagreed.

The majority of my peers said, this is a terrible idea because all youre going to do is lend some legitimacy to some of these strange products and websites that are out there. Theyre going to say, you know, this product is under investigation by Dr. Bedlack at Duke and this team of respected scientists, and theyre right. said Bedlack.

But he thought the potential good outweighed the risks.

I just feel like you have to put it all together and ask yourself: How does it all shake out? To me, the need for this in the patient community, the desire for it, far outweighs any of that criticism that I got in the beginning.

In 2009, Bedlack connected a cohort of like-minded researchers to create ALSUntangled a group dedicated to investigating alleged or emerging ALS treatments that spring up online.

What if we work together,? What if we crowdsource this? Like, built a team of clinicians and scientists who were interested in doing this together.

Together, they dug into one of the groups first product reviews: Iplex, a drug that contained a man-made insulin-like growth factor whose dysregulation has long been thought to be involved in ALS. ALSUntangled concluded that data from a seemingly promising Italian study lacked a control group and was potentially tainted with selection bias.

The problem with that is the time that it takes to really investigate one thing. It takes a while, Bedlack said. Ive found that it takes about 40 hours to do a really good investigation of just one product. And, nobody has time, if theres hundreds of these things out there, which there are, nobody has time to do them all.

Since that first review, the ALSUntangled team has grown to over 130 researchers across 11 countries.

Since 2009, there hasnt been a single day that I havent at some point been working on a review of a product that a patient asked about, said Bedlack.

ALSUntangled has reviewed dozens of products and therapies keeping the information up to date whenever new evidence becomes available.

Most have been relatively unremarkable, some pretty dangerous. But a minority have actually shown real promise.

The work has given Bedlack and his team permission to wander down strange paths, just to see where they might lead. And now one of the strangest of paths of them all may finally be paying off.

Two years after publishing that first ALSUntangled review, Bedlack stumbled across yet another seemingly unreliable internet rumor related to ALS.

I came across a video of a woman from Virginia who said that she had ALS, that it was rapidly progressing, that she had lost almost all of her function.

Her name is Nelda Buss a mother of two whose ALS journey began in the mid-80s, when she told her primary care doctor about some foreboding, mysterious symptoms she was experiencing.

It started with my weak hands, said Buss. And then my legs sort of were getting weak. I fell a couple of times. I went back to him and he said, Well, Ill make the neurology appointment like in January.

Buss believed her doctor didnt want to be the one to give her the bad news. She was officially diagnosed with ALS when she was 47. By then she was having difficulty walking.

My husband got up, came up and picked me up. And I think we cried all the way home.

Buss consulted with ALS experts some of the best in the business at the time, according to Rick Bedlack. But she just kept getting worse.

I was diagnosed in January and by July I was in a wheelchair, said Buss.

Desperate, she sought help from Dean Kraft, a man from New York City who claimed to be an energy healer. She had heard about him from a magazine article.

The first time I went to him he gave me the first treatment and my diaphragm was beginning to weaken and I couldnt breathe as well as I could before, Buss told the hosts of the daytime talk show The View back in 1998. And I noticed I could cough and blow my nose better.

Every other week for over a year, Buss and her husband would drive up to New York City from their home in Virginia, where she was carried into Dean Krafts small office. Kraft would place his hands above Buss head and claim to release healing energy.

He would work like two hours on Saturday on me and two hours on Sunday. said Buss.

In total, Buss said she paid Kraft about $25,000 for these sessions.

He said, you just cant always believe the doctors, said Buss.

The first time I went to him he gave me the first treatment and my diaphragm was beginning to weaken and I couldnt breathe as well as I could before, Buss told the hosts of the daytime talk show The View back in 1998. And I noticed I could cough and blow my nose better.

Every other week for over a year, Buss and her husband would drive up to New York City from their home in Virginia, where she was carried into Dean Krafts small office. Kraft would place his hands above Buss head and claim to release healing energy.

He would work like two hours on Saturday on me and two hours on Sunday. said Buss.

In total, Buss said she paid Kraft about $25,000 for these sessions.

He said, you just cant always believe the doctors, said Buss.

Dean Kraft died in 2013 of a massive heart attack. He was 63. Kraft was also featured in the same segment from the View and other videos about Buss story.

I dont require people to believe in religion, he told the hosts. They dont even have to believe in me. I just lay my hands on them and fortunately the majority of people get well.

And after a couple of years, Buss said thats what happened to her.

I had a walking party at the Marriott hotel and invited all our friends, so I had Dean come to the party. So they came down from New York and he wanted me to dance with him.

Rick Bedlack was shocked when he came across the story of Nelda Buss.

She completely recovered and in fact the video was pretty convincing, said Bedlack.

Again, the doctors curiosity kicked in. He contacted Buss and asked if she would give permission for her doctors to send Bedlack her medical records.

She obliged.

By the time I finished those, I was absolutely convinced that she really did have ALS, that she progressed to where she was nearly dead, and then she made a full recovery over the next two years under the care of this energy healer, said Bedlack. What I wasnt convinced of is that it was the energy healing that made her better, in part because it had no plausible mechanism. Like, there is no known biological mechanism where a person can have energy come out of their hands that heals the body dying motor neurons. And so I didnt understand that part.

Bedlack reached out to Kraft to try to organize a study of his methods.

[I] said,I dont know how it is that this happened, but Id like to do a small study of your technique and about 10 more patients. And Ill never forget his response. He said, Richard, for those who believe no more proof is necessary. And for those who dont, no proof is ever going to be enough. And thats the last I ever heard of him.

But the story started a conversation within ALSUntangled about other inexplicable disease reversals his fellow researchers had seen.

They said, did you know these kinds of cases have actually been reported in the literature since the 1960s? And in fact, many of the people on the ALSUntangled team had said, well, you know, I saw somebody that I thought had ALS and they progressed for a while and then they recovered.

His colleagues said they just thought those patients had been misdiagnosed that they didnt really have ALS. But for Bedlack, this was a light bulb moment.

And I was like, Wait a second. How are we not studying these people? How many of them are there? I mean, theres a precedent for studying people who are unexpectedly resistant to diseases and finding pathways that have never been manipulated and finding treatments to manipulate those pathways that wind up helping everyone. said Bedlack.

So Bedlack started yet another program to study these reversal cases. He began digging out medical records, sending out questionnaires, and trying to find commonalities.

Suddenly Im in a whole other direction for the past 12, 13 years, this whole ALS reversals research. But I have to say thats also gotten quite interesting.

Bedlack has confirmed 22 other ALS reversals. And just last year, his searching spawned a breakthrough.

We actually found a target, said Bedlack. About a third of these patients appear to have a genetic abnormality thats very, very rare in people with typically progressive ALS. I think thats the most likely explanation for at least a third of these ALS reversals. And we are now doing a much larger study to see in a huge population of people with ALS: is there a relationship? If there is a relationship, I will be dropping just about everything and engaging in a clinical trial. But again, here I am in a space in a direction that I never thought I would be.

Nelda Buss is now 82 years old and she still believes Dean Kraft saved her life. But she remains open to other explanations, assuming Rick Bedlack and his tireless team of researchers can find one.

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Switching From S1P-Modulating Therapies to Other DMTs – Neurology Live

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At the 2024 Consortium of Multiple Sclerosis Centers (CMSC) Annual Meeting, NeurologyLive sat down with MS expert Donald Negroski, MD, to discuss several of the top presentations and data on treatment switches and aging in MS. Negroski provided an overview of various presentations, offering his clinical perspective and how findings may impact care going forward.

In this segment, Negroski provided commentary on a retrospective analysis highlighting the reasons for switching from sphingosine 1-phosphate (S1P)-modulating agents to ozanimod (Zeposia; BMS), another FDA-approved disease-modifying therapy. In addition, he spoke on the financial toll some patients face when choosing between approved therapies.

Transcript edited below for clarity.

Donald Negroski, MD: In the abstract, they (investigators) asked healthcare providers why patients switched from the various S1Ps to ozanimod, and the major driver was actually copay assistance and some financial issues with lack of copay as well as tolerability less so. The take-home message is that copay assistance and financial burden on patients is starting to drive treatment decisions, which is something unusual. In the past, neurologists have seemed to think thatand rightly sothey know who should go on what particular drugs and some of these recent abstracts suggest that there's other drivers, more from a financial standpoint.

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Roche, Ascidian to develop gene therapies for neurological diseases – LabPulse

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Roche has announced a research collaboration and licensing agreement with biotech firm Ascidian Therapeutics to develop gene therapies for neurological diseases.

According to the terms of their agreement, Roche will pay Ascidian $42 million upfront for exclusive, target-specific rights to use Ascidian's RNA exon-editing technology to develop therapeutics for undisclosed neurological diseases, the firms said in a statement. Furthermore, Roche will pay Ascidian up to $1.8 billion in total as research, clinical, and commercial milestones are reached. Ascidian is also eligible to receive royalties on commercial sales worldwide for any therapies that are developed under the collaboration.

Under their arrangement, Ascidian will be responsible for conducting discovery and certain preclinical activities in collaboration with Roche, and Roche will be responsible for certain other preclinical activities, as well as further clinical development, manufacturing, and commercialization, Ascidian said. While Roche will have exclusive rights to the technology for the targeted diseases, Ascidian can pursue other disease targets outside of its agreement with Roche.

Boston-based Ascidian's exon-editing technology is designed to correct the RNA produced by damaged exons, the regions of DNA containing the blueprints to make proteins. Correcting the RNA produced by damaged exons greatly mitigates the risks associated with direct DNA editing and gene replacement, such as off-target edits, Ascidian said.

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Roche, Ascidian to develop gene therapies for neurological diseases - LabPulse

University of Colorado Anschutz Medical Campus Receives $2 Million Gift from the Cline Dion Foundation to Advance … – PR Newswire

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The investment will fund the Celine Dion Foundation Endowed Chair in Autoimmune Neurology at CU Anschutz

AURORA,Colo., June 18, 2024 /PRNewswire/ -- TheUniversity of Colorado Anschutz Medical Campus announced the creation of the Celine Dion Foundation Endowed Chair in Autoimmune Neurology, made possible by a $2 million philanthropic investment from the Celine Dion Foundation.

The investment will fund initiatives to advance research inautoimmune neurological disorders, such as stiff person syndrome (SPS), and support Amanda Piquet, MD, associate professor ofneurologyat theUniversity of Colorado School of Medicine, who has been named the inaugural chairholder. Piquet specializes in diagnosing, treating and advancing research for SPS, a rare, chronic and progressive autoimmune neurologic disease characterized by muscle stiffness, painful spasms and difficulty walking.

Piquet is also the director of theAutoimmune Neurology Program at CU Anschutz, where the program's mission is to provide the best neurological care and improve the well-being of patients with an autoimmune neurological disorder.

Celine Dion, who has been deeply committed to advancing healthcare for all, was diagnosed with SPS in 2022 and is an advocate forsupporting all who have been affected by the disease. Dion is being treated for SPS by Piquet at UCHealth University of Colorado Hospital on the CU Anschutz Medical Campus.

The disease currently has no cure but can be managed with symptomatic and immune therapies to make quality of life better.

This gift will help boost this field of study and expedite research discoveries, ensuring that individuals receive the most informed treatments as they become available. To enable this vision, this investment will support the following key priorities:

"SPS and other rare autoimmune neurological disorders can be difficult to diagnose and treat because they often affect individuals differently. This generous gift from the Celine Dion Foundation and the overall increased awareness for SPS will change the future of not only diagnosing the disease but will catapult research efforts to explore new approaches of treatment," said Piquet.

The $2 million investment will be provided to the campus over the next five years and allow Piquet to build upon her current success treating patients with rareautoimmune neurological disorders.

About the University of ColoradoAnschutz Medical CampusThe University of Colorado Anschutz Medical Campusis a world-class medical destination at the forefront of transformative science, medicine, educationand patient care. The campusencompassesthe University of Colorado health professional schools, more than 60 centers and institutes, and two nationally ranked independenthospitals-UCHealth University of Colorado HospitalandChildren's Hospital Coloradowhich see more than 2 million adult and pediatric patient visits yearly. Innovative, interconnected and highly collaborative, the University of Colorado Anschutz Medical Campusdelivers life-changingtreatments, patient care and professional training and conducts world-renowned research fueled by $705 million in research grants.For more information, visitwww.cuanschutz.edu.

Contact: Julia Milzer, University of Colorado Anschutz Medical Campus, 303-725-0733,[emailprotected]

Find the latestUniversity of Colorado Anschutz Medical Campus news here.

SOURCE University of Colorado Anschutz Medical Campus

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New study suggests cancer drug could be used to target protein connection that spurs Parkinson’s disease – EurekAlert

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image:

Neurons express Aplp1 (in white), a key protein that allows brain cells to absorb Parkinsons-disease causing alpha-synuclein.

Credit: Yasuyoshi Kimura, Ph.D.

FOR IMMEDIATE RELEASE

In studies with genetically engineered mice, Johns Hopkins Medicine researchers say they have identified a potentially new biological target involving Aplp1, a cell surface protein that drives the spread of Parkinsons disease-causing alpha-synuclein.

The findings, published May 31 in Nature Communications, reveal how Aplp1 connects with Lag3, another cell surface receptor, in a key part of a process that helps spread harmful alpha-synuclein proteins to brain cells. Those protein buildups are hallmarks of Parkinsons disease.

Notably, the researchers say, Lag3 is already the target of a combination cancer drug approved by the U.S. Food and Drug Administration (FDA) that uses antibodies to teach the human immune system what to seek and destroy.

Now that we know how Aplp1 and Lag3 interact, we have a new way of understanding how alpha-synuclein contributes to the disease progression of Parkinsons disease, says Xiaobo Mao, Ph.D., associate professor of neurology at the Johns Hopkins University School of Medicine and a member of the Institute for Cell Engineering. Our findings also suggest that targeting this interaction with drugs could significantly slow the progression of Parkinsons disease and other neurodegenerative diseases.

Mao co-led the research along with Ted Dawson, M.D., Ph.D., Leonard and Madlyn Abramson Professor in Neurodegenerative Diseases at the Johns Hopkins University School of Medicine and director of the Johns Hopkins Institute for Cell Engineering, Valina Dawson, Ph.D. and Hanseok Ko, Ph.D., professors of neurology at the school of medicine and members of the Institute for Cell Engineering.

Long-standing studies have shown that by clumping together and forming protein deposits, misfolded alpha-synuclein proteins journey from brain cell to brain cell, killing those responsible for producing a neurotransmitter called dopamine, and causing Parkinsons disease to progress through a type of programmed cell death that Johns Hopkins researchers have identified. The process, parthanatos (from the Greek word for death), leads to impairments in movement, emotional regulation and thinking.

Aplp1s bond with Lag3 on the cells surface enables healthy brain cells to absorb traveling clumps of alpha-synuclein, leading to cell death, the researchers say.

In mouse studies published in 2016 and 2021, Mao and Dawsons team identified Lag3s role in binding with alpha-synuclein proteins, causing Parkinsons disease to spread. However, those studies indicated that another protein was partially responsible for the cells absorption of misfolded alpha-synuclein.

Our work previously demonstrated that Lag3 wasnt the only cell surface protein that helped neurons absorb alpha-synuclein, so we turned to Aplp1 in our most recent experiments, says Valina Dawson.

To determine whether Aplp1 indeed contributed to the spread of harmful alpha-synuclein proteins, researchers used a line of genetically engineered mice lacking either Aplp1 or Lag3 or both Aplp1 and Lag3. In mice without Aplp1 and Lag3, cell absorption of the harmful alpha-synuclein protein dropped by 90%. After injecting mice with the Lag3 antibody, they found that this drug also blocks the interaction of Aplp1 and Lag3, meaning healthy brain cells could no longer absorb disease-causing alpha-synuclein clumps.

The researchers say the Lag3 antibody nivolumab/relatlimab, a drug FDA approved in 2022 for cancer treatment, could play a role in preventing cells from absorbing alpha-synuclein.

The anti-Lag3 antibody was successful in preventing further spread of alpha-synuclein seeds in the mouse models and exhibited better efficacy than Lag3-depletion because of Aplp1s close association with Lag3, Ted Dawson says.

This research has potential applications in treating other neurodegenerative conditions that have no cures, Mao says. In Alzheimers disease, which is associated with symptoms of memory loss, mood instability and muscle problems, tau proteins become misfolded and clump together in neurons at high levels, worsening the condition. In Alzheimers research, Mao says scientists could try to target Lag3 which also binds with the dementia-related tau protein with the same antibody.

With the success of using the Lag3 antibody in mice, Ted Dawson says the next steps would be to conduct anti-Lag3 antibody trials in mice with Parkinsons disease and Alzheimers disease. The Johns Hopkins researchers are also looking into how they could prevent unhealthy cells from releasing disease-causing alpha-synuclein in the first place.

Other researchers on this study are Hao Gu, Donghoon Kim, Yasuyoshi Kimura, Ning Wang, Enquan Xu, Ramhari Kumbhar, Xiaotian Ming, Haibo Wang, Chan Chen, Shengnan Zhang, Chunyu Jia, Yuqing Liu, Hetao Bian, Senthilkumar Karuppagounder, Fatih Akkentli, Qi Chen, Longgang Jia, Heehong Hwang, Su Hyun Lee, Xiyu Ke, Michael Chang, Amanda Li, Jun Yang, Cyrus Rastegar, Manjari Sriparna, Preston Ge, Saurav Brahmachari, Sangjune Kim, Shu Zhang, Haiqing Liu, Sin Ho Kweon, Mingyao Ying and Han Seok Ko from Johns Hopkins; Yasushi Shimoda from the Nagaoka University of Technology; Martina Saar and Ulrike Muller from Heidelberg University; Creg Workman and Dario Vignali of the University of Pittsburgh School of Medicine and Cong Liu of the Chinese Academy of Sciences.

This work was supported by grants from the National Institutes of Health (R01NS107318, R01AG073291, R01AG071820, 1135 RF1NS125592, K01AG056841, R21NS125559, R01NS107404, P01AI108545, R01AI144422), the Parkinsons Foundation, the Maryland Stem Cell Research Foundation, the American Parkinson Disease Association, the Uehara Memorial Foundation, the JPB Foundation, the Adrienne Helis Malvin Medical Research Foundation, and the Parkinsons Disease Foundation.

DOI: 10.1038/s41467-024-49016-3

Nature Communications

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New study suggests cancer drug could be used to target protein connection that spurs Parkinson's disease - EurekAlert

Neurology Devices Market Size 2024 Analysis by Market Dynamics, Industrial Trends, Developments and Forecast till … – openPR

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Latest Report, titled "Neurology Devices Market" Trends, Share, Size, Growth, Opportunity and Forecast 2024-2031, by Coherent Market Insights offers a comprehensive analysis of the industry, which comprises insights on the market analysis. The report also includes competitor and regional analysis, and contemporary advancements in the market.

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The report sheds light on the competitive landscape, segmentation, geographical expansion, revenue, production, and consumption growth of the Neurology Devices market. The keyword Market Size, Growth Analysis, Industry Trend, and Forecast provides details of the factors influencing the business scope. This report provides future products, joint ventures, marketing strategy, developments, mergers and acquisitions, marketing, promotions, revenue, import, export, CAGR values, the industry as a whole, and the particular competitors faced are also studied in the large-scale market.

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B. Braun Melsungen AG Boston Scientific Corporation BIONIK Laboratories Corp. Integra LifeSciences Holdings Corporation Johnson and Johnson Magstim Co Ltd. Braintale SAS Medtronic Abbott Zimmer Biomet Stryker Corporation Helius Medical Technologies Inc. Avanos Medical Inc. W.L. Gore & Associates Inc. HeadsafeIP Pty Ltd. Cerus Endovascular Ltd. Cyberonics Inc

This Report includes a company overview, company financials, revenue generated, market potential, investment in research and development, new market initiatives, production sites and facilities, company strengths and weaknesses, product launch, product trials pipelines, product approvals, patents, product width and breath, application dominance, technology lifeline curve. The data points provided are only related to the company's focus related to Neurology Devices markets. Leading global Neurology Devices market players and manufacturers are studied to give a brief idea about competitions.

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By Device Type: CSF Management devices(CSF Shunt Devices, CSF Drainage Devices)Interventional Neurology Devices(Neuro Thromobectomy, Cerebral Balloon Angioplasty & Stents,Aneurysm Coiling, Support Devices)Neuro-surgery Devices(Neuro-endoscopes, Sterotactic- Systems, Ultrasonic- Aspirators, Aneurysm Clips) Neuro-stimulation Devices(Spinal Cord Stimulation, Deep Brain Stimulation, Sacral Nerve Stimulation, Vagus Nerve Stimulation,Gastric Nerve Stimulation) By End User: Hospitals, Ambulatory surgery centers, Others

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This report is centred around the Neurology Devices in the worldwide market, with a specific focus on North America, Europe, Asia-Pacific, South America, Middle East, and Africa. The report classifies the market by manufacturers, regions, type, and application. It presents a comprehensive view of the current market situation, encompassing historical and projected market size in terms of value and volume. Additionally, the report covers technological advancements and considers macroeconomic and governing factors influencing the market.

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The report examines the key opportunities in the Neurology Devices Market and identifies the factors that are driving and will continue to drive the industry's growth. It takes into account past growth patterns, growth drivers, as well as current and future trends.

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Questions Answered by the Report:

(1) Which are the dominant players of the Neurology Devices Market? (2) What will be the size of the Neurology Devices Market in the coming years? (3) Which segment will lead the Neurology Devices Market? (4) How will the market development trends change in the next five years? (5) What is the nature of the competitive landscape of the Neurology Devices Market? (6) What are the go-to strategies adopted in the Neurology Devices Market?

About Author:

Ravina Pandya, Content Writer, has a strong foothold in the market research industry. She specializes in writing well-researched articles from different industries, including food and beverages, information and technology, healthcare, chemical and materials, etc. (https://www.linkedin.com/in/ravina-pandya-1a3984191)

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Coherent Market Insights is a global market intelligence and consulting organization focused on assisting our plethora of clients achieve transformational growth by helping them make critical business decisions. We are headquartered in India, having sales office at global financial capital in the U.S. and sales consultants in United Kingdom and Japan. Our client base includes players from across various business verticals in over 57 countries worldwide. We create value for clients through our highly reliable and accurate reports. We are also committed in playing a leading role in offering insights in various sectors post-COVID-19 and continue to deliver measurable, sustainable results for our clients.

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Neurology Devices Market Size 2024 Analysis by Market Dynamics, Industrial Trends, Developments and Forecast till ... - openPR

Roche and Ascidian enter neurological disease partnership worth over $1.8bn – PMLiVE

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Roche and Ascidian Therapeutics have partnered to develop RNA exon editing therapies for neurological diseases, with the deal worth over $1.8bn.

The research collaboration and licensing agreement gives Roche exclusive, target-specific rights to Ascidians RNA exon editing technology for undisclosed neurological targets.

Ascidian will conduct discovery and certain preclinical activities in collaboration with Roche, which will be responsible for further preclinical work as well as clinical development, manufacturing and commercialisation.

In exchange, Ascidian will receive an initial payment of $42m and will be eligible to receive up to $1.8bn in research, clinical and commercial milestone payments, plus royalties on global commercial sales.

More than three billion people worldwide were living with a neurological condition in 2021, according to a new major study released earlier this year by The Lancet Neurology.

Among the top ten neurological conditions contributing to loss of health in the same year were stroke, neonatal encephalopathy, dementia, diabetic neuropathy, epilepsy and nervous system cancers.

Ascidian said its technology allows for the therapeutic targeting of large genes and genes with high mutational variance while maintaining native gene expression patterns and levels. The approach is designed to provide the durability of gene therapy and reduce the risks associated with direct DNA editing and gene replacement.

James Sabry, global head of pharma partnering at Roche, said: Our partnership with Ascidian is an opportunity to harness advanced RNA exon editing technology, which has the potential to deliver transformative one-time therapeutics by editing multiple whole exons at the RNA level with a single treatment.

Also commenting on the alliance, Michael Ehlers, Ascidians president and chief executive officer, said: The potential of treating disease by large-scale exon editing of RNA is vast.

We look forward to working with the Roche team to develop first-in-class RNA exon editing medicines for multiple neurological diseases, with a mission and passion to relieve suffering and improve lives.

The partnership comes just one week after Roche entered into a strategic licence agreement for the use of ALZpaths pTau217 antibody to develop and commercialise a diagnostic blood test for Alzheimers disease.

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Roche and Ascidian enter neurological disease partnership worth over $1.8bn - PMLiVE

Roche and Ascidian Therapeutics Collaborate on Treatments for Neurological Diseases – Pharmaceutical Technology Magazine

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The research collaboration and licensing agreement will focus on the discovery and development of RNA exon editing therapeutics.

Ascidian Therapeutics, a biotechnology company developing treatments by rewriting RNA, announced on June 18, 2024 that it has signed a licensing agreement with Roche to collaborate on the discovery and development of RNA exon editing therapeutics to treat neurological diseases (1). The collaboration will combine RNA exon editors with Roches next-generation central nervous system (CNS) delivery capabilities. Ascidian enables precise post-transcriptional editing of genes by editing exons at the RNA level.

As part of the agreement, Ascidian will receive an initial payment of $42 million with up to $1.8 billion in research, clinical, and commercial milestone payments, including commercial royalties. The partnership will allow Ascidian to create internal and collaborative programs within the neurology area. Roche will receive exclusive, target-specific rights to Ascidians RNA exon editing technology and will perform certain preclinical activities. Roche will also be responsible for further clinical development, manufacturing, and commercialization.

Roche is known and respected worldwide for their expertise in complex neurological diseases, and I am proud of the scientific rigor and quality of the work done at Ascidian that has led to this partnership, Michael Ehlers, MD, PhD, president and chief executive officer of Ascidian Therapeutics, said in a press release. The potential of treating disease by large-scale exon editing of RNA is vast. We look forward to working with the Roche team to develop first-in-class RNA exon editing medicines for multiple neurological diseases, with a mission and passion to relieve suffering and improve lives.

Our partnership with Ascidian is an opportunity to harness advanced RNA exon editing technology, which has the potential to deliver transformative one-time therapeutics by editing multiple whole exons at the RNA level with a single treatment, James Sabry, MD, PhD, global head of Pharma Partnering at Roche, said in the release.

In May 2024, Ascidian presented preclinical data that enabled the clearance of an investigational new drug (IND) application through Phase I/II testing for its RNA exon editor, ACDN-01, at the American Society of Gene & Cell Therapy (ASGCT) annual meeting in Baltimore, Md. FDA granted ACDN-01 Rare Pediatric Disease Designation as well as Fast Track Designation.

ACDN-01 is the only clinical-stage therapeutic targeting the genetic cause of Stargardt disease, and we look forward to sharing the preclinical data that led to its IND clearance, along with the plans for the first-in-human trial, said Ehlers in a press release (2). ACDN-01 is designed to overcome challenges that have long kept Stargardt disease out of reach and to provide persistent therapeutic benefit with one dose. Our progress with ACDN-01 speaks to its therapeutic potential in Stargardt disease and the broader promise of our RNA exon editing platform to significantly expand the possibilities of RNA medicines.

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Roche and Ascidian Therapeutics Collaborate on Treatments for Neurological Diseases - Pharmaceutical Technology Magazine

Study aims to understand genetics of Parkinsons disease in Black people – The Source – Washington University in St. Louis

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Erin Foster, an associate professor of occupational therapy, and Scott Norris, MD, an associate professor of neurology, have established a site at Washington University School of Medicine in St. Louis for the Black and African American Connections to Parkinsons Disease (BLAAC PD) study, an international study aimed at understanding the gene changes that may lead to Parkinsons disease in people with African ancestry. Parkinsons is a neurodegenerative disease characterized by slow and unsteady movement. Foster and Norris are collecting clinical and behavioral data from people with Parkinsons and healthy people who identify as Black or African American in the St. Louis area.

By joining the study, Washington University also joins the Parkinsons Genetics Program, a global initiative geared at promoting a more comprehensive view of Parkinsons disease by collecting genetic data from 150,000 people representing diverse populations around the world. Parkinsons is a debilitating disease that affects people of all backgrounds, but it has historically been understudied in many populations, including Black, Latino, Asian, Native American, LGBTQ+, those in lower socioeconomic groups and people living in underserved geographies (rural and urban).

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Study aims to understand genetics of Parkinsons disease in Black people - The Source - Washington University in St. Louis

Hidden Sex Differences In Neurological Reward Pathways Suggest Opportunity For Improved Psychiatric Therapeutics – UMBC News

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A new study in the Journal of Neuroscience has discovered underlying sex differences in the molecular pathways that drive reward-related behaviors. In particular, the study found differences and similarities in the ways males and females strengthened connections between two brain regionsthe hippocampus and the nucleus accumbensinvolved in reward signaling.

Males and females both suffer from disorders involving these pathways, like depression and substance abuse. However, the presentation and prevalence of these conditions can differ between the sexes, and certain standard treatments are more effective on average in males or females. The new papers findings encourage further research to determine if the molecular differences the authors discovered may underpin differences in disease progression or medication response, which could eventually lead to more effective treatments for mental health disorders.

Although this is changing, historically, much more research has been done on male subjects (both in humans and animal models), so we just dont know a lot about female brains and differences between male and female brains, says Tara LeGates, assistant professor of biological sciences and senior author on the new paper. Shes seen an increase in the number of research groups considering sex differences, and is hopeful that their work will continue to produce actionable results that lead to improved outcomes for patients.

LeGates previous work used optogenetics, which allows researchers to selectively stimulate particular neurons with light, to demonstrate that strengthening connections between two brain regionsthe hippocampus and nucleus accumbensis rewarding for mice. The hippocampus is best known for its roles in memory and learning, as well as emotional responses. The nucleus accumbens is a key reward center that integrates information from different brain regions to drive goal-oriented behavior, LeGates explains.

The hippocampus-nucleus accumbens pathway also exists in humans, and is involved in reward processes in the same way as in mice, LeGates notes, making this research highly translatable to human studies.

The researchers used electrophysiology, which involves observing how living cells respond to stimulation of other brain regions under a microscope, to reach their conclusions about how males and females strengthen connections between the hippocampus and nucleus accumbens.

LeGates and lead author Ashley Copenhaver, a Ph.D. candidate in LeGates research group, found that mice of both sexes relied on activation of a particular kinase protein, CAMKII, to facilitate reward-related behavior. Neither sex required dopamine activation, which was surprising, because dopamine is commonly involved in reward-related signaling.

The neurotransmitter receptor NMDA is also commonly involved in reward pathways and strengthening connections between brain regions. The researchers found that male mice were using NMDA receptors to strengthen connections between the hippocampus and nucleus accumbens, but females were not. Instead, the females used a different channel for calcium ions and an estrogen receptor.

We were really surprised to find this sex difference, Copenhaver says. Because the NMDA receptor pathway is so commonly assumed to be at play, It was just really fascinating to see, not only are males and females using different mechanisms, but one is using this NMDA receptor-dependent mechanism, whereas females are not, Copenhaver says. Theyre using this other, non-canonical pathwaythese alternative calcium ion channels. We werent expecting that at all.

Revealing these differences and similarities is an important step toward making a real difference in medical care for patients.

If you want to understand susceptibility and develop better treatments, you have to understand the mechanisms at these synapses, LeGates says. You have to understand whats happening, and you have to understand it in each of the sexes.

Legislation required human studies to include males and females in the early 1990s, but not until 2015 did the National Institutes of Health set policy that animal studieswhich are frequently used to justify further human researchmust also include both sexes. As a result, there are still many open questions about how male and female physiology differs, and many opportunities to make contributions with significant biomedical impact.

LeGates became more interested in studying sex differences in brain function during her postdoctoral fellowship at the University of Maryland School of Medicine. I think that one of the problems with trying to do sex difference research is that youre trying to use things that have been optimized to work in male animals, LeGates says, and then when it doesnt play out in females, its just like, Oh, its unreliable. But what if its that the tests were optimized in males, and thats why they dont work in females?

I wanted to pursue that and appreciate the male and female differences and not try to force them into the same exact paradigms, she adds. Maybe we need to come up with new paradigms and a new way to approach how we study them.

Tags: Biology, CNMS, GradResearch, Research

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Hidden Sex Differences In Neurological Reward Pathways Suggest Opportunity For Improved Psychiatric Therapeutics - UMBC News

These Signs of Memory Loss Could Actually Predict Alzheimer’s Brain Changes – SciTechDaily

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A recent study revealed that individuals who self-report memory problems, corroborated by their partners, have higher levels of tau tangles, a key Alzheimers disease biomarker. This correlation suggests that early detection of memory issues could be crucial for effective intervention, especially with the advent of new treatments.

Early memory complaints, validated by partners, are linked to increased tau tangles in the brain, emphasizing the potential of early Alzheimers detection and intervention.

Individuals who report early memory problems and whose partners also suspect they have memory problems have higher levels of tau tangles in the brain, a biomarker associated with Alzheimers disease. This is according to a study published in the May 29, 2024, online issue of Neurology, the medical journal of the American Academy of Neurology.

Subjective cognitive decline is when a person reports memory and thinking problems before any decline is large enough to show up on standard tests.

Understanding the earliest signs of Alzheimers disease is even more important now that new disease-modifying drugs are becoming available, said study author Rebecca E. Amariglio, PhD, of Harvard Medical School in Boston. Our study found early suspicions of memory problems by both participants and the people who knew them well were linked to higher levels of tau tangles in the brain.

675 adults with an average age of 72 who did not have cognitive impairment on formal testing participated in the study. All had brain scans for amyloid plaques. Of this group, 60% had elevated levels of amyloid, meaning they were at risk for developing cognitive impairment due to Alzheimers disease even though, at the time of the scan, they were cognitively normal. Participants did not know if they had elevated levels of amyloid.

Each participant had a study partnera spouse, child, or friendwho could answer questions about the participants thinking and memory skills and ability to perform daily tasks. In 65% of cases, partners lived with participants.

Each participant and their partner completed a questionnaire to assess the participants subjective cognitive decline. Questions included, Compared to one year ago, do you feel that your memory has declined substantially? and Compared to one year ago, do you have more difficulty managing money? Participants and partners scores were recorded with higher scores indicating greater complaints about memory.

Researchers also reviewed brain scans for levels of tau tangles. Greater tau is also a risk factor for Alzheimers disease and is at higher levels in people with elevated amyloid.

The scientists found that participants with higher levels of tau tangles in the brain had higher scores of complaints on the memory questionnaire. Their partners also scored them higher. This association was stronger in participants who had elevated levels of amyloid plaques.

Our study included a high percentage of people with elevated amyloid, and for this reason, we were able to also see that memory complaints were associated with higher tau tangles, said Amariglio. Our findings suggest that asking older people who have elevated Alzheimers disease biomarkers about subjective cognitive decline may be valuable for early detection. This is particularly important since it is predicted that treatments given at the earliest diagnosable form of the disease will be the most effective in slowing the disease.

Limitations of the study include that most participants were white and highly educated. Amariglio noted future studies should follow people for longer periods of time and include more participants from other racial and ethnic groups, as well as people with different levels of education.

For more on this research, see Memory Complaints Can Predict Biological Changes in the Brain.

Reference: Associations Between Self and Study Partner Report of Cognitive Decline With Regional Tau in a Multicohort Study by Michalina F. Jadick, Talia Robinson, Michelle E. Farrell, Hannah Klinger, Rachel F. Buckley, Gad A. Marshall, Patrizia Vannini, Dorene M. Rentz, Keith A. Johnson, Reisa A. Sperling and Rebecca E. Amariglio, 29 May 2024, Neurology. DOI: 10.1212/WNL.0000000000209447

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These Signs of Memory Loss Could Actually Predict Alzheimer's Brain Changes - SciTechDaily

Long COVID Brain Fog: Impact and Coping Strategies – Neuroscience News

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Summary: Long COVID, affecting 7% of U.S. adults, often includes debilitating brain fog. Symptoms like forgetfulness and difficulty focusing affect daily life and work. A new study highlights that while brain fog often resolves, it significantly impacts mental function. Effective coping strategies and treatments are crucial for managing this condition.

Key Facts:

Source: Yale

Brain fog is one of the most debilitating problems experienced by people withLong COVID, a condition in whichCOVID-19-like symptoms continue or develop after the acute infection has passed.

People who experience brain fog say they have an inability to think clearly, are forgetful, and cant focus their attention or find the right words in a conversation.

An estimated 7% of adultsor about 17 million peoplein the United Statesreported having Long COVIDin March 2024, based ondatafrom the Centers for Disease Control and Prevention (CDC).

Estimates vary as to exactly how many of those people struggle with cognitive function, but in one study of people with Long COVID, close to half reported having poor memory or brain fog.

For most people, Long COVID brain fog eventually goes away, but it still can have a life-altering impact.

Its definitely not subtle, says neurologistLindsay McAlpine, MD, who directs the Yale Medicine NeuroCovid Clinic and works with neurologistSerena Spudich, MD, MS, to research Long COVID-related cognitive dysfunction.

People have told me they used to be amazing at multitasking, but with brain fog they can do only one thing at a time. Other patients have switched jobs because they could no longer handle the tasks, stress, or thought-load of their previous job.

There is no cure for Long COVID or brain fog, but experts are learning more about how to care for patients who have it, Dr. McAlpine adds.

Below, Yale Medicine and Yale New Haven Health providers answer questions about Long COVID brain fog and what to do about it.

Brain fog isnt an official medical diagnosis; rather, its a colloquial term for a range of significant, persistent neurocognitive impairments that cause such symptoms as sluggish thinking, difficulty processing information, forgetfulness, and an inability to focus, pay attention, or concentrate.

With Long COVID, the exact combination of brain fog symptoms varies from one person to the next.

The condition can affect anyone who has had COVID, regardless of their age or the severity of their initial COVID infection.

Brain fog is considered a Long COVID symptom if its present three months after the person had COVID and has persisted for more than two months, Dr. McAlpine says. It usually goes away completely between six and nine months after the infection, although in some people it lasts as long as 18 months or more, Dr. McAlpine says.

Scientists dont yet have a solid understanding of what causes Long COVID brain fog. One theory is that the SARS-CoV-2 virus that causes COVID persists in the gut after the acute infection has cleared up, and changes in the gut have been associated with changes in brain function.

Dr. McAlpine also cited asmall studypublished in February 2024 inNature Neurosciencethat used a specialized type of MRI (called dynamic contrast-enhanced magnetic imaging) to show that some Long COVID patients with brain fog have dysregulation in the blood-brain barrier, a network of tissue and blood vessels that protects the brain from harmful substances.

There is no single test to confirm that a person has Long COVID, and the same is true for brain fog. But a neurological exam and cognitive testing can identify deficits in a persons brain function.

Similarly, there is no specific cognitive screening test for people with Long COVID, but a number of tests used to evaluate conditions like dementia can help determine whether a person is experiencing it, Dr. McAlpine says.

We look for deficits in language, working memory, declarative memory [a type of long-term memory], motor function, and perception, she says.

It helps to know if a patient has other Long COVID symptoms, which are wide-ranging and can include fatigue, difficulty breathing, heart palpitations, headache, stomach pain, and joint pain, among others, she adds.

Yes, some people develop new conditions when they have Long COVID; the condition can also worsen existing conditions and unmask diseases that were there previously but undiagnosed, Dr. McAlpine says.

This is why the patients story and clinical history really matter, because if the brain fog doesnt link up with COVID, then we have to think about different causes, she says.

Bloodwork, including a complete blood count and comprehensive metabolic panel, helps rule out such problems as a thyroid condition or vitamin B-12 deficiency that are known to cause cognitive symptoms.

Syphilis andhuman immunodeficiency virus (HIV)are also conditions to test for, depending on the patients risk for those conditions, Dr. McAlpine says.

Obstructive sleep apnea (OSA)is another potential cause for cognitive dysfunction, and is often diagnosed in people with Long COVID, Dr. McAlpine says. Or they had sleep apnea before and it was tolerable for them, but after COVID they became much more sensitive to it and had more symptoms.

Likewise, a subset of patients in Dr. McAlpines practice had either diagnosed or undiagnosedattention-deficit/hyperactivity disorder (ADHD)before COVID, and Long COVID caused a dramatic worsening of their ADHD symptoms, including the forgetfulness and lack of focus also associated with brain fog, she says.

Some found that the medication they had been taking for ADHD stopped working for them, she says.

Ive also cared for people who had always suspected they had ADHD, but they were high-functioning and coped. Their coping skills stopped working with Long COVID.

There are other conditions, such aschronic fatigue syndrome, andpostural orthostatic tachycardia syndrome (POTS), that are associated with cognitive dysfunction independent of Long COVID.

In individuals with brain fog who have these syndromes as part of their Long COVID, the brain fog may not improve until we address these conditions, Dr. McAlpine says.

Long COVID brain fog clears up in the majority of people who have it, but lifestyle practices can help, Dr. McAlpine says. For instance, exercise is one thing we know boosts cognition in everybody, even in patients with dementia.

Maintaining healthy sleep routines, staying hydrated, minimizing alcohol intake, and avoiding tobacco also help, she says.

There is also a mood component, which is important, Dr. McAlpine adds, explaining that many people with brain fog symptoms also experience depression oranxiety, and those who had mental health conditions before may notice them getting worse. But, if a mental health problem is diagnosed, it needs treatment.

In addition, Dr. McAlpine says many of her patients have responded well to two medicationsN-acetylcysteine (NAC) and guanfacine.

In 2020,Arman Fesharaki-Zadeh, MD, PhD, a Yale Medicine behavioral neurologist and neuropsychologist, discovered that the medications could help Long COVID patients with brain fog, when he realized that one of his Long COVID patients was having cognitive symptoms that were similar to patients with a history of traumatic brain injury (TBI) who were suffering from post-concussive syndrome.

NAC was being tested for the treatment of TBI and also helped with cognitive deficits. He added guanfacine, which was developed by Yale neuroscientistAmy Arnsten, PhD, and had been used to treat ADHD.

The two published asmall studyin the Nov. 2023 issue ofNeuroimmunology Reports, and now researchers are hoping for funding for larger clinical trials. In the meantime, NAC is available over-the-counter, and patients may be able to get a prescription for guanfacine off-label from their doctor.

There has also been evidence ofCOVID vaccineshelping with Long COVID symptoms like brain fog, but there are no guarantees, Dr. McAlpine says.

We had many patients in our first wave of COVID who had bad brain fog after COVID, and their symptoms improved with their first vaccination. But Ive seen that happen less lately, possibly because more people are vaccinated. That may have been more of a first wave phenomenon.

While some people experience more severe brain fog than others, many find there are strategies that can help, says Kaleigh Frame, MA, CCC-SLP, a Yale New Haven Health speech-language pathologist who has cared for Long COVID patients who have already been seen by a Yale Medicine neurologist. She provides strategies based on the types of cognitive deficits they are struggling with.

First, she teaches patients to build self-advocacy skills, such as letting other people know about their limitations due to brain fog. She also helps with metacognition, which she describes as a persons ability to assess their own cognitive skills.

For instance, they decide how they are doing at different times on a scale of 1 to 10 and record their numbers on a calendar or notes app.

This can help determine whether there are patterns of brain fog throughout the day, and it can also help track progress or decline, she says.

Then, the next time you follow up with your neurologist, it wont be vague, because you have a written log you can refer to.

Yet another strategy is having a brain budget, which involves estimating how much mental energy you have in a given day (based on your records) and prioritizing when and how to best use it, making sure you have time for breaks so your brain power is not used up too quickly. A person might say, I can do all six of these things, but in between, I need recovery breaks, Frame says.

Frame also has specific advice for the following brain fog issues:

Its impossible to predict whether someone will develop Long COVID and/or brain fog. Long COVID occurs more often in people whose COVID illness was severe, those who had underlying health conditions before their infections, and people who are unvaccinated, according to the CDC.

But people with mild infections have had Long COVID symptoms as well, and Dr. McAlpine has had otherwise healthy patients in their 20s and 30s whove experienced brain fog.

If you have brain fog, its important to get treatment, says Frame. While everyone is different, both Frame and Dr. McAlpine say treatment and support can help in many cases.

Author: KATHY KATELLA Source: Yale Contact: KATHY KATELLA Yale Image: The image is credited to Neuroscience News

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Long COVID Brain Fog: Impact and Coping Strategies - Neuroscience News

New AI tool may help detect early signs of dementia – UT Southwestern

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Dementia, an impaired ability to remember, think, or make decisions, mainly affects people over 65. But early recognition can be clinically challenging. (Photo credit: Getty Images)

DALLAS May 30, 2024 A novel speech analysis tool that uses artificial intelligence successfully detected mild cognitive impairment and dementia in a Spanish-speaking population, according to research led by UTSouthwestern Medical Center. The study, published in Frontiers in Neurology, provides preliminary support for the algorithm as an early screening tool that may help identify patients at risk of developing dementia.

Dementia is an impaired ability to remember, think, or make decisions that mainly affects adults older than 65, but it is not a normal part of the aging process. Currently, anestimated 6.9 million people in the U.S. have Alzheimers disease, which is the most common cause of dementia. Early recognition of cognitive decline presents a clinical challenge but is a critical part of classifying patients with the highest risk of dementia.

C. Munro Cullum, Ph.D., Professor of Psychiatry, Neurological Surgery, and Neurology and Vice Chair and Chief of the Division of Psychology at UT Southwestern, holds the Pam Blumenthal Distinguished Professor in Clinical Psychology.

Analyzing a sample of speech obtained during some brief, routine neuropsychological tests shows promise in our ability to quickly screen for signs of cognitive impairment, particularly in population-based research studies. Machine learning-based tools such as this may play an increasingly important role in the future of cognitive screening for dementia, said corresponding author C. Munro Cullum, Ph.D., Professor of Psychiatry, Neurological Surgery, andNeurology and Vice Chair and Chief of the Division of Psychology at UTSouthwestern. Dr. Cullum is also an Investigator with the Peter ODonnell Jr. Brain Institute.

Data for the study was collected from 195 Spanish speakers recruited as part of a multicenter clinical trial in Spain. All participants completed an initial evaluation and were categorized as either having normal cognition, mild cognitive impairment (MCI), or dementia. Data from 21 participants was excluded due to incomplete cognitive or demographic data, or poor audio transcription quality.

The final cohort of 174 participants had a mean age of 74; there were slightly more females (56%) than males. Participants were divided into a training group of 122 participants (70%) and a test group of 52 participants (30%).

Researchers used four language tasks to train independent machine learning (ML) models using data from the training group participants. Neuropsychological performance and audio recording variables were collected from each participant using the AcceXible platform a proprietary web-based instrument developed for disease detection through speech analysis.

The final model of the speech analysis algorithm was then used for the test group and was able to differentiate cognitively normal participants from those with dementia or MCI with an overall accuracy of 88.4% and 87.5%, respectively. The final model outperformed one of the current standard-of-care screening measures known as the Mini-Mental State Examination (MMSE).

Findings from this study andsimilar work with English speakers by UTSW researcher Ihab Hajjar, M.D., Professor of Neurology andInternal Medicine and in the ODonnell Brain Institute, suggest that these tools may improve quality of life for patients at risk for dementia through early detection an issue that most significantly affects marginalized racial and ethnic groups who often experience delayed diagnosis. Further research is needed to validate the accuracy of the model before the technology can be deployed for clinical use.

Eventually, such technology may help identify patients who are showing signs of cognitive decline that may be in need of clinical evaluation and consideration for treatment, Dr. Cullum noted.

Other UTSW researchers who contributed to this study include first author Alyssa N. Kaser, graduate student in clinical psychology; Laura Lacritz, Ph.D., Distinguished Teaching Professor of Psychiatry and Neurology;Leslie Rosenstein, Ph.D., Associate Professor of Psychiatry; Emmanuel Rosario Nieves, Ph.D., Assistant Professor of Psychiatry; Jeffrey Schaffert, Ph.D., Assistant Professor of Psychiatry; and Holly Paxton-Winiarski, Ph.D., postdoctoral fellow in Neuropsychology.

Dr. Cullum holds the Pam Blumenthal Distinguished Professor in Clinical Psychology. Dr. Hajjar holds the Pogue Family Distinguished University Chair in Alzheimers Disease Clinical Research and Care, in Memory of Maurine and David Weigers McMullan.

About UTSouthwestern Medical Center

UTSouthwestern, one of the nations premier academic medical centers, integrates pioneering biomedical research with exceptional clinical care and education. The institutions faculty members have received six Nobel Prizes and include 25 members of the National Academy of Sciences, 21 members of the National Academy of Medicine, and 13 Howard Hughes Medical Institute Investigators. The full-time faculty of more than 3,100 is responsible for groundbreaking medical advances and is committed to translating science-driven research quickly to new clinical treatments. UTSouthwestern physicians provide care in more than 80 specialties to more than 120,000 hospitalized patients, more than 360,000 emergency room cases, and oversee nearly 5 million outpatient visits a year.

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New AI tool may help detect early signs of dementia - UT Southwestern

Recognizing the Clinical Features of MOGAD for Diagnosis: Eoin P. Flanagan, MB, BCh – Neurology Live

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WATCH TIME: 4 minutes

"One thing we were highlighting is that in MOGAD, it doesn't tend to form scars, and the lesions often resolve, which is very different from MS."

Myelin oligodendrocyte glycoprotein (MOG)-associated disease (MOGAD) is a rare antibody-mediated inflammatory demyelinating disorder of the central nervous system. Although the clinical presentation of MOGAD might resemble neuromyelitis optica spectrum disorder (NMOSD), most experts regard it as a distinct condition with a different immune system pathology than NMOSD. MOG is a molecule on the outer membrane of myelin sheaths expressed in the brain, spinal cord, and optic nerves. Research shows that the specific outmost location of myelin makes it a potential target for autoimmune antibodies and cell-mediated responses in the demyelinating processes.1

Accurate diagnosis of MOGAD relies on the identification of pathogenic MOG antibodies in the patients serum using precise and sensitive methods, preferably with optimized cell-based assays (CBA) as recommended by researchers.1 MRI imaging can also aid in distinguishing MOGAD from other neuroinflammatory disorders such as multiple sclerosis (MS) and NMOSD. Despite the limited randomized controlled trials in MOGAD, reported observational data suggest that high-dose steroids and plasma exchange may help to treat acute attacks. Additionally, immunosuppressive therapies such as steroids, oral immunosuppressants, and rituximab are recommended by clinicians as a treatment for managing MOGAD.

Eoin P. Flanagan, MB, BCh, professor of neurology and chief of the Division of Multiple Sclerosis and Autoimmune Neurology at Mayo Clinic, presented on diagnostic clinical pearls for MOGADat the 2024 Consortium of Multiple Sclerosis Centers (CMSC) Annual Meeting, held May 29 to June 1, in Nashville, Tennessee. At the meeting, Flanagan, who also serves as the director of the Autoimmune Neurology Fellowship, sat down in an interview with NeurologyLive to discuss the key differences between MOGAD and MS in terms of lesion formation and resolution. He also spoke about how spinal fluid testing can be useful in diagnosing MOGAD when serum tests are inconclusive. In addition, he spoke about the current state of treatment options for MOGAD compared with NMOSD.

Click here for more coverage of CMSC 2024.

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What to Know About the Rising Stroke Rates in Younger People – Health Matters

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What health problems are contributing to the increase in stroke among younger people? Dr. Willey: The main ones elaborated on in the CDC report and ones we have seen from other studies are a rise in obesity, physical inactivity, diabetes, and high blood pressure in younger people. This is translating to earlier cardiovascular disease and stroke, as the report outlines. In terms of high blood pressure, for example, it has been estimated that if it is treated, it would help prevent 50% of strokes in the U.S.

Other than cardiovascular conditions and obesity, the opioid overdose epidemic may also be contributing to the rise in young people. There has been an increase in intravenous (IV) opioid use, and IV drug use is linked to infections in heart valves that can cause strokes.

Are the signs of stroke in younger people similar to those in older people? The symptoms of stroke in both younger and older patients tend to be similar, though young patients outcomes tend to be better because at baseline, they have a better physical status, such as fitness and mobility. Since stroke tends to be less common in those who are younger, symptoms could be mistaken for a migraine, pinched nerves, or multiple sclerosis.

What are the different kinds of strokes? There are two major types of strokes. One of them is ischemic, which is like a blocked pipe. When this occurs, blood is not getting to a certain part of the brain and that part of the brain dies. There is also a hemorrhagic stroke, which is when the arteries burst.

In the U.S., ischemic stroke is about 80% of all strokes, though there is significant differences by communities. Communities that have higher rates of high blood pressure and social determinants of health are more likely to present with hemorrhagic stroke. This kind of stroke has a higher chance of being fatal compared to an ischemic stroke. Patients with this type of stroke present uniformly with a severe onset, rapid headache, often an impairment of consciousness, which you do not necessarily see with other types of stroke.

Younger patients tend to have different types of stroke but for the most part, the rates of hemorrhagic strokes and ischemic strokes remain the same. One notable exception is pregnancy-related strokes, where hemorrhagic ones can be more likely.

If someone is having a stroke, what can people keep in mind in terms of improving outcomes? Most people can identify signs and symptoms of a heart attack, but not for stroke, so it is important to be familiar with them.The acronym BE FAST covers most stroke symptoms. In 2021, the AHA endorsed a version of BE FAST in Spanish: RPIDO. It is important to emphasize that if someone has these symptoms, and they only lasted a few minutes, it could be a sign that a bigger stroke is about to come. People should still come to the hospital as quickly as possible.

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What to Know About the Rising Stroke Rates in Younger People - Health Matters