Catherine Rydell, CEO of the American Academy of Neurology (AAN), said she never felt qualified for any of her jobs but believes in raising your hand and saying yes to opportunities. Yet when she retires in May, her 21-year tenure will be one of the longest among Minnesota nonprofit leaders.

Before joining the AAN, she was a volunteer leader as a stay-at-home mom who then became a state legislator in North Dakota. She believes that empowering her staff and giving them opportunities of their own is how the AAN has become the largest association for neurologists, with 36,000 members.

Mary Post, executive director of the American Board of Anesthesiology, will take over for Rydell.

Q: How is the AAN of 2020 different from the organization you were chosen to lead in 1999?

A: In 1999, I became the third executive director and the first woman to hold the position. When I arrived, the board had just approved its first strategic plan but was focused more on operations. With the help of some key board members, we were able to evolve the governing body to be much more strategically focused. As programs and services for members grew, we expanded staff, led by a competent and innovative executive team. Continual strategic planning has become the norm, backed by data, member input and environmental scans, which tip us off to new trends and concerns. This enables us to be more proactive, rather than reactive, which is critical in the rapidly shifting health care environment.

Q: How has the field of neurology changed in 20 years and what demands has that placed on AAN?

A: The AAN was founded in 1948 by Dr. A.B. Baker, who chaired the neurology department at the University of Minnesota. He started it to provide support and continuing medical education to young neurologists who were going into practice.

That need for support, not only for practicing neurologists but for those in academic institutions and in research, has significantly grown as the health care environment has become more complicated and challenging.

Today, the AAN has more than 36,000 members with 28,000 of those in the U.S. and serves as the worlds largest association of neurologists to help the one in six people worldwide affected by neurologic disease, such as stroke, Alzheimers disease, migraine, Parkinsons disease, concussion, MS, and epilepsy.

Our education and science programs at our annual meetings attract as many as 15,000 attendees. We advocate in Washington, D.C., to reduce the administrative burdens that regulations place on our practicing neurologists. We also advocate for increases in funding for the National Institutes of Health and the BRAIN Initiative so we can speed up the cures and treatments needed for more than 600 brain diseases. And we also help our academic neurologists find greater efficiencies and improvements in care for their patients.

Q: How has membership changed in the last 20 years?

A: One of the most significant aspects is that we have very strong retention rates among our U.S. members, currently at 95%. Our members feel they are getting their moneys worth from the AAN, and 83 cents of every dollar in dues goes back to our members in the form of benefits, programs and services. We represent 93% of all neurologists in the U.S. And we have more than 8,000 members from 141 countries.

We have also taken a more holistic approach to recognizing that the neurologist is a member of a care team. Its becoming more the norm that when you see a neurologist, you first see an advanced practice provider who has training in neurology fundamentals and can provide more of the basic services before the neurologist comes to the exam room. We now have more than 1,400 advanced practice providers as members, and we have tailored education programs for them. We also have 300 neurology business administrators as members; they fill the crucial role of keeping our members practices running efficiently, and we have programs and services to help them in their clinics and institutions.

We have seen more women come into neurology, from 29% of our membership in 2008 to 40% in 2019. Women and minority neurologists still face obstacles in the workplace because of gender and race. AAN has developed training programs to address those challenges, and we have created leadership programs to ensure that the leadership of the AAN and neurology in general is broad-based and representative.

Q: How have the publication and convention businesses contributed to the growth of the organization. How have they grown and why are they important to the membership and organization?

A: Members receive our eight publications, including the Neurology medical journal and Brain & Life magazine for patients (its free for the public) as either a membership benefit or a deeply discounted subscription rate. The revenue from our publications is a significant portion of our total revenue, which helps us keep member dues low and provide neurologists the services they need.

Our signature event of the AAN since 1949 has been our annual meeting, which has grown to become the worlds largest gathering of neurology professionals, with over 15,000 attendees. The last time we held our annual meeting in Minneapolis was in 1998, for our 50th anniversary. Since then, we have grown too large for the number of hotel rooms the downtown area can provide. However, this summer we will be holding our Sports Concussion Conference here and expect as many as 500 attendees.

Our meetings not only bring together the best and brightest experts to teach, inform and inspire attendees, they also offer networking opportunities and camaraderie.

Q: Tell us about your successor and the challenges she and the organization will likely face in the next 20 years.

A: Mary Post was selected based on her extensive experience as a CEO of the American Board of Anesthesiology (ABA), as well as her broad experience at the American Academy of Neurology, where she served for 16 years (19922008) in many leadership roles, including a deputy executive director. We are happy to have Mary come home.

Q: What are next steps for you: traditional retirement or an encore career?

A: Im truly looking forward to spending more time with family, friends, and enjoying lake life. But I also know that I am intrigued by a challenge. As they say, never say never.

Patrick Kennedy 612-673-7926

Follow this link:
One of longest tenured nonprofit CEOs retiring on a strong note - Minneapolis Star Tribune

Article In Brief

Investigators reported that acute sleep loss alters diurnal profiles of plasma-based Alzheimer's disease biomarkers in the cerebrospinal fluid of healthy young men.

Blood serum levels of a protein linked to Alzheimer's disease (AD)total tau (t-tau)rose significantly after just one night of acute sleep loss in healthy young men, according to a new report published in the January 8 online edition of Neurology.

What is notable is that the present and similar findings have been demonstrated in young, healthy individuals, study investigator and author Jonathan Cedernaes, MD, PhD, told Neurology Today. Taken together with evidence that sleep loss at an earlier age seems to be somewhat predictive of the risk of later developing Alzheimer's disease, we believe this at least provides an indication that even young individuals should take care of their sleep.

Dr. Cedernaes noted that the evidence suggests it may also be important for those who are already at risk for AD due to genetic factors, for instance, to optimize their sleep.

One should also not forget that many other factors can be important for prevention of AD, such as diet and exercise, so all of these factors need to be considered to promote a healthy lifestyle in general, he added.

Dr. Cedernaes, a senior researcher in the neuroscience department at Uppsala University in Sweden, and his colleagues conducted a within-subject, crossover-design study with 15 healthy men in their early 20s who participated in two standardized in-lab sessions with two different conditionsone night of normal sleep and one night of overnight sleep deprivation. The researchers then measured levels of t-tau and another biomarker of AD, amyloid beta (Abeta-40 and Abeta-42), before and after each overnight session. In addition, in order to investigate biomarkers of neuroaxonal injury, the researchers also assessed levels of neurofilament light chain (NfL), a protein found in axons that is released following white matter injury and degeneration, as well as glial fibrillary acidic protein (GFAP), which is elevated in AD.

They found that the evening-to-morning change in average plasma levels of t-tau increased following sleep loss, compared with normal sleep (p=0.0345). When the researchers examined whether sleep loss would alter overnight changes in plasma levels of Abeta, they observed no significant evening-to-morning changes in levels of Abeta-40 (p=0.24) or Abeta-42 (p=0.76) following acute sleep loss compared with sleep.

In addition, they found significant evening-to-morning decreases in Abeta-42 (-17.1 percent; p<0.0001) and GFAP in plasma (-12.1 percent; p<0.0001) regardless of sleep condition.

These findings could indicate that these proteins are controlled by a biological clock mechanismthat they exhibit so-called diurnal or circadian rhythms, Dr. Cedernaes said.

Dr. Cedernaes explained that the decrease in Abeta-42 and GFAP can provide insight into how the brain's biological clock controls either production or clearance of proteins involved in regulating the health of neurons and glial cells.

Given that other groups have found that sleep loss increases levels of Abeta-42 in the cerebrospinal fluid (CSF) of older individuals, for example, our findings may also involve changes in peripheral mechanisms that clear these proteins once they exit the central nervous system, or alternatively, our findings may represent changes that are only seen in younger, but not older individuals, he said.

There were no significant differences between the two experimental conditions in terms of how they impacted the evening-to-morning change in plasma levels of the neuroaxonal damage markers NfL (p=0.26) or GFAP (p=0.48).

One major limitation of the study was the small, homogenized sampleall were young white men in good health. Thus, the findings may not be generalizable to older people, women, or those who are already at higher risk of worse brain health due to a medical condition such as diabetes, Dr. Cedernaes said.

Future research would ideally examine whether similar changes in biomarkers for AD might occur in response to other types of sleep restriction, such as recurrent partial sleep loss, Dr. Cedernaes said, as this may provide information about how loss of sleep may promote the types of changes shown in the study.

We are also interested in establishing how these biomarkers are regulated by circadian rhythms, and whether changes are similar in individuals affected by health conditions such as obesity or type 2 diabetes, which have been found to increase the risk of dementia, he noted.

These findings should be viewed as an exploratory analysis, which needs to be confirmed in larger populations and under different settings of disrupted sleep and circadian rhythms, such as in a chronic simulation of the sleep/wake schedule that a shift worker may experience, Dr. Cedernaes wrote.

He noted that another research group using a sample of similar size also found an increase in t-tau in response to sleep loss, but they had measured the increase in subjects' CSF.

A growing number of studiesboth experimental and epidemiologicalsuggest that sleep is intertwined in the pathogenesis in AD, said Dr. Cedernaes. What is unclear at present, in humans at least, is the extent to which disrupted sleep and circadian rhythms contribute to the pathogenesis of this condition. The alternative, which research also supports, is that AD also disrupts sleep and circadian rhythms. Both of these mechanisms are often hypothesized to be at play in what we refer to as a bidirectional mechanism.

The findings are intriguing and improve our understanding of the diurnal dynamics of serum AD biomarkers, said Diego Carvalho, MD, a sleep medicine fellow at Mayo Clinic in Rochester, MN. As sleep is important for the clearance of toxic metabolic by-products and downscaling of synaptic connections, sleep loss could contribute to higher tau levels by decreased glymphatic activity and increased release of tau from greater neuronal activity with lower synaptic efficiency, he noted.

Sleep loss has also been associated with neuroinflammation, which could further contribute to tau release. Further research should assess whether serum tau could predict longitudinal tau accumulation under the condition of chronic sleep restriction.

AD researcher Barbara Bendlin, PhD, associate professor of medicine at the University of Wisconsin-Madison, noted that a growing body of literature suggests that sleep abnormalities impact the brain. Sleep abnormalities have been linked with AD pathology, and vice versa. Understanding how sleep loss impacts the brain is important because this may be a modifiable risk factor for the development of AD, she said.

She noted that several biomarkers previously assessed in the context of AD and other neurological diseases were examined, including markers related to amyloid, tau, glial activation, and neurodegeneration.

That plasma tau is elevated following a night without sleep is quite interesting; previous studies from Washington University in St. Louis have found a link between sleep and tau pathology in animal models as well as among older adults. However, more work is needed to establish whether and how elevated tau levels at younger ages may contribute to later-life neurodegenerative disease, Dr. Bendlin noted. She said that inclusion of women in a future study would improve the generalizability of the results, particularly given the increased risk of AD among women.

This small, exploratory study in 15 healthy young men is well-designed and builds on previous work looking at the effect of acute sleep loss on amyloid-beta and tau in CSF, said Brendan P. Lucey, MD, assistant professor of neurology and director of the sleep medicine section at Washington University School of Medicine.

For instance, we found that one night of sleep deprivation increases CSF Abeta by about 30 percent and tau by about 50 percent. This study suggests that plasma tau is affected by sleep deprivation whereas other proteins, such as Abeta, are not. Although these results need to be replicated, the study has implications for tracking the effect of sleep on Abeta and tau using plasma rather than CSF for screening or clinical trials. Future studies with more participants, women, and older adults are needed, he said.

Drs. Cedernaes, Carvalho, Bendlin, and Lucey had no competing interests.

The rest is here:
Acute Sleep Loss in Healthy Young People Is Linked to... : Neurology Today - LWW Journals

COLORADO SPRINGS, Colo. -- Every 12 weeks, Shannon Stone goes to her neurologist to get Botox injected in and around her head. Not for cosmetic reasons, but for chronic migraines.

Ive been working with Stone for chronic migraines, said Dr. Andrea Manhart, a neurologist at UCHealth Colorado Springs. Shes gone from approximately daily migraines to three per month.

The whole process takes no more than five minutes and only needs to be done every few months.

It has really changed the world of neurology, Dr. Manhart said of Botox, a product normally associated with cosmetics and reducing wrinkles.

Stone gets Botox injected into 31 injection sites.

To be a candidate for Botox, you have to have more than 15 migraine headache days for a month and you have to fail three of the oral preventative therapies, Dr. Manhart said.

Stone fit that criteria.

Every migraine medication that they would give me was failing, or the side effects would be too bad to where I couldnt continue the medication any longer, Stone said.

To even begin to understand Stones pain, you have to know her story. She started getting migraines in 2002 and found Botox as a solution two years ago. Stone and her doctors believed the migraines stemmed from a car accident in 2002.

I fractured three vertebrae in my neck and the windshield went through the right side of my face, Stone explained. So, the healing of all of that just caused a lot of neurological and muscle and tissue damage.

It was a bad accident, we barely survived, said Robert McCall, Stones 17-year-old son.

Stone was nine months pregnant with McCall during the accident and as he grew up, he took on more of a role in the family to help when Stone was in pain.

I had to cook dinner a lot of the time and make sure my sisters got whatever they had to do for the night, homework and take a bath and stuff, McCall said.

There would be times where they would last for like three or four days at a time with minimal breaks, Stone said.

When Botox was presented to her as an option, her first fear was that her eyes would get droopy one of the side effects Dr. Manhart explained.

I never wanted to let any of my friends or people that I knew know that I was receiving Botox because I didnt want them to judge me or feel like I was doing it for a beauty type of thing, Stone said.

The FDA approved Botox as a treatment for chronic migraines back in 2010.

Botox is for a specific person, it is for a specific chronic migraine patient, Dr. Manhart said.

A study done by the American Society of Plastic Surgeons showed that three months after injection, patients treated with Botox had an average of 1.6 fewer migraine attacks per month.

How Botox works is relatively unknown but the theory is that it de-activates pain receptors in the brain to reduce neurotransmitters that send pain signals to the brain, Dr. Manhart said.

For Stone, its helped her spend more time with her kids.

You can really see an improvement in her and just her overall appearance, McCall said. She doesn't look down all the time, shes not always sleeping.

I can still move my eyebrows, I can still move my face, I just cant make an angry face, Stone said.

Follow this link:
Botox used as alternative solution for chronic migraines - The Denver Channel

Article In Brief

A telerobotic system for endovascular care, in the early phases of development, could provide stroke treatment in remote and hard-to-reach places.

A bedside robotic unit and a remote physician workspace, allowing real-time surgery to be controlled from a remote location, may well represent a future strategy for providing endovascular care for stroke in remote and hard-to-reach places, suggests a paper published in late November 2019 in the Journal of Neurosurgery.

Although more institutions are now able to provide endovascular care than ever before, there is also a greater need for comprehensive care teams to deliberate on the complex questions about pathology and symptomatology after patients' initial presentations, Gavin W. Britz, MD, MBA, MPH, professor and chair of the department of neurological surgery, and colleagues from Houston Methodist Hospital, wrote in the paper.

These resources can be hard to find in hospitals that do not see a large enough volume of such patients, they noted. The use of telemedicine and teleoperated robots may offer a potential solution for disseminating interventional stroke care to smaller regional or rural centers, they said.

The cockpit-like design of the system allows a physician to sit at a remote radiation-shielded workstation and use a set of touchscreen controls and joysticks that are then translated to the movements of the local robotic device.

The robotic unit features an extended reach arm, a robotic drive mechanism, and a single-use cassette containing all the necessary endovascular tools, including angiographic and hemodynamic monitors and foot pedalcontrolled fluoroscopy.

The software for the system, which was cleared by the US Food and Drug Administration in 2018, was initially developed for endovascular percutaneous coronary intervention (PCI) procedures.

A 2019 study in EClinicalMedicine reported that it had successfully demonstrated the system's use for PCI in five individuals from a 20-mile distance. And a feasibility study by Dr. Britz and colleagues in Neurosurgery last June demonstrated the device's ability to navigate the cerebrovascular system, manipulate the guidewires and microcatheters routinely used for endovascular intervention, and successfully deploy coils and stents in a live animal.

But while the use of telemedicine and teleoperated robots may bridge the gaps in interventional stroke care in smaller regional or rural centers, operational and financial challenges remain, independent stroke and neurovascular care experts said. They told Neurology Today they look forward to a future where this technology would be safe, effective, and feasible, but said that it was much too early to consider this a viable reality.

Indeed, the authors of the current study acknowledged the high cost of the device would be a potential barriercoming in at $650,000 per unit, with another $650-$750 for its single-use accessory cartridgesin addition to the investment needed to hire and train the surgical technicians and other operating room staff. They suggested that non-tertiary hospitals may be able to spread out some of those expenses between cardiovascular and neuro-interventional services, however.

The study authors acknowledged that there was still a lot of work to be done before the system would be ready for primetime, including performing preliminary trials of intracranial endovascular procedures such as angiography, coilings, and stent deployments in humans safely as a proof of capability.

Tests of the system need to be performed to mirror a range of potential scenarios in multiple subjects with diverse anatomical locations and complexities, the study authors wrote. In addition, Remote procedures would need to be performed in coordination with locations where adequate contingency options (such as experienced neuro-interventionalists) also exist onsite, they added.

Only then, by studying the metrics and outcomes of robotically performed procedures and comparing them to those of the hub-and-spoke or diffused care models, can a decision be made regarding the efficacy of the device and its capability to address deficiencies in the status quo, Dr. Britz and colleagues concluded, adding, however, that they believe these hurdles can be overcome.

In an accompanying editorial, Jeffrey T. Nelson, MD, and Nicholas C. Bambakidis, MD, both from the University Hospitals Cleveland Medical Center, acknowledged the relevance of future research into the development of neuroendovascular robotics. But they said its use as a solution to our current access issues in the delivery of stroke care seems premature....If and when a telerobotic neurointerventional procedure is available, it may prove to be a useful adjunct to stroke treatment if the technical limitations are overcome. For now, we must continue to develop systems of stroke care that provide access to all patients with acute ischemic stroke.

Independent experts who spoke with Neurology Today agreed that these interventions were an exciting prospect but they were far from ready for widespread use.

The challenge of making endovascular thrombectomy more accessible to patients living in rural areas is very complex as the number of patients who would be treated locally at a small rural hospital is not sufficient to support an interventionalist, Carolyn A. Cronin, MD, PhD, associate professor of neurology and director of the vascular neurology fellowship program at the University of Maryland School of Medicine, acknowledged. This article presents a novel idea to respond to that challenge, she said.

However, Dr. Cronin added, Even if the interventionalist could be off-site, there are still many resources that would be needed locally and also may be cost-prohibitive. These include a fully capable endovascular suite with biplane imaging, technicians familiar with neurointerventional procedures and all the different devices in use, and an interventionalist to obtain vascular access.

She added that supplementary training would be necessary for the neurointerventionalists who would be using the robotic equipment in order to ensure they would be equally as competent with the procedures remotely as they are in person which is a time and cost consideration.

Telerobotic surgery would be an intriguing potential option but needs further study regarding both the safety and quality of the intervention done remotely and also whether it would be financially viable, Dr. Cronin concluded.

Pooja Khatri, MD, MSc, FAAN, professor of neurology at the University of Cincinnati (UC) and co-director of the UC Stroke Team, agreed that the article was very intriguing and did a good job of laying out the currently available evidence and pros and cons of telerobotic stroke intervention.

The concept of using telerobotics for mechanical embolectomy makes intuitive sense, compared to open surgery, when one considers that the operator is already using a screen to guide his or her work even in person. But much more work is to be done before we get there, she cautioned.

The technical tradeoffs for the operator seem to be tactile feedback for mechanical precision, and early data from cardiac trials suggest that these tradeoffs might not sacrifice technical safety or efficacy. The question will be whether the same will be true in the brain. The brain has more twists and turns in arteries, and more to lose with delays and complications.

Dr. Khatri said an important factor will be the availability of stable, strong, and fast internet connections at all participating centers.

It is exciting to consider the advantages of these systems, Dr. Khatri said, including expedited access for patients in much more remote areas to a highly effective and highly time sensitive treatment.

There are many questions that need to be answered before this can happen, however, including: Who sets up the procedure and takes the first steps? Who steps in when there are procedural failures and complications?

As the editorial lays out nicely, the need to expand access to neurointerventional care is urgent and the road to development of telerobotics is relatively long. We can't wait for telerobotics to expand our workforce and resources for acute stroke care, Dr. Khatri said.

At the same time, even with an adequate workforce and resources countrywide, the authors make a compelling case for robotics enhancing care even when the interventionist is there in person.

Dr. Khatri said she was looking forward to seeing the data from these technologies in humans with stroke.

Drs. Britz, Khatri and Cronin had no relevant disclosures to report.

More here:
Are Telerobotic Devices the Answer to Stroke Care... : Neurology Today - LWW Journals

In the study, 85% (99/116) of children with life-threatening autoimmune conditions had complete or near complete recovery after biomarker was spotted and they were subsequently given appropriate treatment

A group of life-threatening neurological conditions affecting children have been linked to an antibody which points to potential treatment, according to an observational multicentre study involving 535 children with central nervous system (CNS) demyelinating disorders and encephalitis, published in The Lancet Neurology journal.

The findings suggest that the myelin oligodendrocyte glycoprotein (MOG) antibody is associated with a wider range of life-threatening autoimmune conditions than previously thought, including neuromyelitis optica spectrum disorders and encephalitis, which cause severe neurological (brain and nervous system) symptoms such as vision loss, muscle weakness, and loss of coordination and speech.

Because this group of CNS disorders can mimic similar conditions like multiple sclerosis (MS), they are difficult to diagnose correctly. Until around 10 years ago, patients with these demyelinating diseases were considered to have atypical forms of MS, and the prognosis and best treatment options were unknown. Over the last 10 years, multiple studies have shown that several demyelinating diseases (including optic neuritis, myelitis, and acute disseminated encephalomyelitis [ADEM]) associate with the MOG-antibody biomarker, and patients affected by this group of diseases frequently improve with immunotherapy. However, the best treatment approach and long-term outcome remain unknown. Now, this new study suggests that testing for the biomarker could speed accurate diagnosis and help identify the appropriate treatment for some of these disorders.

In the study, 85% (99/116) children who tested positive for MOG antibodies and given appropriate treatment had complete or near complete recovery, but 15% (17) experienced moderate to severe disease-related deficits not caused by the treatment (eg, cognitive impairment, epilepsy, vision loss), and one died from their disease.

"The diagnosis of many of these patients especially those with encephalitis would have been missed if it were not for the prospective design our study," says Dr Thais Armangue from the Sant Joan de Deu Children's Hospital, University of Barcelona, in Spain who co-led the research. "Identifying these patients is important because most of the children who tested positive for MOG antibodies responded to treatment with immunotherapy." [1]

Co-lead author Professor Josep Dalmau from the University of Barcelona explains, "Demyelinating diseases in children can be very difficult to distinguish because they present with similar symptoms and imaging features. Correct and early diagnosis allows for treatment with immunosuppressants, rather than the treatments specifically used in MS that are not effective in most of these diseases. Moreover, it is important to differentiate between those diseases that do not require chronic treatment and others in which prolonged immunotherapy is needed to improve long-term outcomes." [1]

MOG antibodies damage the protective covering (myelin sheath) that surrounds nerve fibres in the brain, optic nerves, and spinal cord, so messages cannot pass along these nerves effectively, causing symptoms such as vision loss, muscle weakness, and pain. Many children may only experience one MOG antibody disease event, and have no further symptoms. However, some children may be at risk of further relapses months, sometimes years, later.

Although there is increasing recognition of MOG-antibody associated syndromes in children, the full range of diseases associated with MOG antibodies remains unknown.

To provide more evidence, researchers conducted a prospective study of children (median age 6 years) with suspected demyelinating syndromes (239 children) and encephalitis other than ADEM (296) attending 40 hospitals across Spain between June 1, 2013, and December 31, 2018. Participants who tested positive for MOG antibodies were assessed for clinical features, response to treatment (ie, number of relapses), and outcomes over a median follow-up of 42 months.

In total, 116 (22%) of 535 children were found to be positive for MOG antibodies, including 94 (39%) with demyelinating syndromes and 22 (7%) with autoimmune encephalitis. Importantly, 24% (28/116) of these children had syndromes not previously associated with MOG antibodies.

Among the 64 patients with autoimmune encephalitis, MOG antibodies were the most frequent biomarkers--more common than all other neuronal antibodies combined (22 [34%] vs 21 [33%])--suggesting that MOG antibody testing should be conducted when diagnosing children with suspected encephalitis after excluding infectious causes, particularly as these patients often respond to treatment with immunotherapy.

The findings also suggest that younger children with MOG-antibody associated syndromes tend to present with clinical features of ADEM (which is an inflammatory condition that mainly affects the brain), whilst older children are more likely to have signs of optic neuritis (eg, loss of vision, pain in the eye) or myelitis (eg, back pain, weakness in both legs).

During follow-up, 33 (28%) of 116 patients positive for MOG antibody disease had relapses. Most of these patients (99/116, 85%) recovered well. However, 17 (15%) experienced disease-related moderate to severe deficits, and one died due to their disease.

"Despite advances in diagnostic testing for encephalitis, up to half of cases have no clear cause. Our findings reveal that the spectrum of MOG antibody disease is broader than previously thought and includes autoimmune encephalitis as well as multiple demyelinating syndromes", says co-author Dr Gemma Olive-Cirera from the Sant Joan de Deu Children's Hospital, University of Barcelona, Spain. "In light of our findings, current classifications and terminology of MOG antibody-associated syndromes should be updated." [1]

The authors note several limitations, including that this was not a registry-based study, and therefore could not assess the incidence or prevalence of MOG antibody-associated syndromes, and that the follow-up was short, which could result in the frequency of relapses being underestimated.

Writing in a linked Comment, Dr Romain Marignier from the Hpital Neurologique Pierre Wertheimer, France (who was not involved in the study) describes the research as "a milestone in the understanding of MOG antibody-associated syndromes", and writes: "In view of the very broad clinical spectrum now associated with MOG autoimmunity, the next challenge will be to identify the optimal therapeutic strategy for each clinical presentation. This objective is closely connected to a better understanding of the pathogenic role of MOG antibodies, and the need for early, robust, and specific prognostic factors of relapse and disability."

Go here to read the rest:
The Lancet Neurology: Discovery could speed diagnosis and treatment of children with life-threatening neurological diseases - Science Codex

Instead of targeting the tricky protein behind Parkinsons, a new compound attacks the RNA that produces it.

Parkinsons disease is a neurodegenerative disorder characterized by tremor, slowness of movement, limb rigidity, and walking and balance issues.

In Parkinsons, a misfolded protein named -synuclein causes the degeneration and destruction of brain cells. The more -synuclein builds up, the more neurons die.

Now, scientists from Rutgers University in New Brunswick, NJ, and Scripps Research in Jupiter, Florida, have developed a way to decrease the amount of -synuclein the body produces.

New technology allowed scientists to identify a compound that shuts down the messenger RNA (mRNA) coding for the destructive protein, preventing the production of -synuclein and the progression of Parkinsons.

The researchers NIH-funded study appears in the Proceedings of the National Academy of Sciences.

According to the Parkinsons Foundation, over 10 million people worldwide are living with Parkinsons disease, with 1 million of those being in the United States.

Each year, about 60,000 U.S. adults receive a diagnosis of the disease.

The incidence of Parkinsons increases with age, although about 4% of people who receive a diagnosis are less than 50 years old. Men are 1.5 times more likely to develop Parkinsons than women.

Currently, there is no cure for Parkinsons disease, and it is truly a devastating disease, says neurology professor M. Maral Mouradian of Rutgers Robert Wood Johnson Medical School Institute for Neurological Therapeutics, and a co-author of the study.

Numerous other approaches have attempted to address the production and buildup of -synuclein, but since the protein has no regular structure and continually changes shape, it has proven difficult to hit with medication.

Several other experimental drugs, says Mouradian, currently being tested for Parkinsons disease are antibodies that target a very late stage of -synuclein protein aggregates.

We want to prevent these protein clumps from forming in the first place before they do damage and lead to advancing disease.

The new research began when Mouradian reached out to chemistry professor Matthew D. Disney of Scripps to explore the potential for a new technology that Disney had invented for matching RNA structures with small-molecules or drug-like compounds.

The scientists had a hunch that they might find a match for the mRNA that coded for -synuclein and that the mRNA might offer a more stable, predictable target than -synuclein itself. The hunch paid off.

For the first time, we discovered a drug-like compound that has the potential to slow down the disease before it advances through an entirely new approach, says Mouradian.

They named their compound Synucleozid, and Mouradian describes it as highly promising.

While Synucleozid may be most effective in people with minimal symptoms and who are in the early stages of Parkinsons, Mouradian says, This new compound has the potential to [] change the course of life for people with this devastating disease.

Synucleozid may be of value beyond Parkinsons since -synuclein has implications in dementia with Lewy Bodies, another progressive condition that affects 1 million people in the U.S. alone.

The study also makes clear the promise of Disneys RNA/protein-matching technology. As Mouradian says, The reach of our study could go beyond people with Parkinsons disease to many other neurodegenerative diseases.

It is a classic example of how interdisciplinary research leads to significant change.

Follow this link:
Parkinson's: Innovative method stops toxic protein buildup - Medical News Today

The mother of a 5-year-old Guatemalan boy sued U.S. Immigration and Customs Enforcement over the medical care he has received in detention for a head injury suffered before the family was arrested.

The lawsuit filed late Friday in California asks a judge to order the child to be taken to a pediatric neurologist or pediatric neurosurgeon. It also seeks to prevent ICE from trying to immediately deport the family.

The boy fell out of a shopping cart in December, fractured his skull and suffered bleeding around his brain. About a month later, he and his family were detained by ICE during what they thought was a routine check-in. The boy, his 1-year-old brother and their mother were taken to ICEs family detention center at Dilley, Texas, while their father was taken to a detention center in California.

The childs relatives and advocates allege thatICE is not properly treating symptomscaused by the accident that began before he was detained. The boy has severe headaches and is hypersensitive to normal levels of sound, according to his aunt and Dr. Amy Cohen, an advocate working with the family. He is also starting to wet himself, according to his aunt. They allege the boys mother has pleaded for medical care, but has been disregarded.

ICE has defended the care the boy has received at Dilley. The agency says medical staff at the detention center conducted multiple check-ups and found no lasting neurological issues. After The Associated Press first inquired about the case on Monday, ICE took the boy to the Childrens Hospital of San Antonio on Tuesday and Wednesday, where he was found to have a normal MRI and no signs of continued bleeding in his skull.

The boy was not seen at the hospital by a pediatric neurologist, according to medical records obtained by his familys attorneys. According to the records, hospital doctors consulted the neurosurgery department and determined that no follow-up was necessary because the MRI was clear.

Cohen said the boy had an appointment to see a neurologist before the family was detained by ICE. The symptoms his family reported began before their detention and could be caused by a head injury even if the initial bleeding is gone, meaning that an MRI would not be enough, she said.

The San Antonio hospital also did not have the paperwork from the California hospital that first treated him, according to the latest records. Doctors at the first hospital determined that the boy needed a neurosurgery follow-up within four weeks.

In a statement Thursday, ICE said it was determined that no issues were present that required the need to elevate the case to another neurological specialist. It declined to comment Saturday on the lawsuit. The Childrens Hospital of San Antonio declined to comment Friday on the case.

The AP is withholding the names of the boy and his family because they fear imminent deportation to Guatemala, where the boys mother says she was threatened.

Originally posted here:
ICE Sued Over Treatment Of 5-Year-Old With Head Injury - KERA News

DUBLIN--(BUSINESS WIRE)--The "Drug Discovery Services Market by Process (Target Selection, Validation, Lead Optimization), Type (Medicinal Chemistry, DMPK), Drug Type (Biologics, Small Molecules), Therapeutic (Oncology, Neurology), Company (Tier 1, 2, 3) - Global Forecast to 2025" report has been added to ResearchAndMarkets.com's offering.

Drug discovery services market to register a CAGR of 12.1% from 2020 to 2025.

The growth of the industry is driven primarily by factors such as growing R&D expenditure in the pharmaceutical & biopharmaceutical industry, increasing demand for outsourcing analytical testing and clinical trial services, initiatives for research on rare diseases and orphan drugs, and focus on drug discovery. Growth in the biologics market and patent expiries will further provide opportunities in the drug discovery services industry. Developing economies are expected to offer a wide range of growth opportunities for players in the market.

The Hit-to-Lead process segment is anticipated to grow at the fastest growth rate during the forecast period.

Based on the process, the drug discovery services market is segmented into target selection, target validation, hit-to-lead identification, lead optimization, and candidate validation. Hit-to-lead identification process is anticipated to be the fastest-growing segment due to the high outsourcing of these services to CROs by the pharmaceutical companies and the emerging advanced technologies for high-throughput screening (HTS) and H2L as well as reductions in development time.

Medicinal Chemistry segment is estimated to account for the largest share of the drug discovery services market in 2020.

Based on type, the drug discovery services market is segmented into medicinal chemistry services, biology services, and drug metabolism and pharmacokinetics (DMPK). The medicinal chemistry services segment is estimated to account for the largest share of the drug discovery services market due to the widespread application of medicinal chemistry in various phases of preclinical drug discovery to deliver robust candidates.

Oncology segment is anticipated to grow at the fastest growth rate during the forecast period.

Based on the therapeutic area, the drug discovery services market is segmented into oncology, cardiovascular diseases, neurology, infectious and immune system diseases, digestive system diseases, and other therapeutic areas. Of all these therapeutic segments, oncology will grow at the fastest CAGR in the drug discovery services market in 2019. The high growth of the oncology segment can be attributed to factors such as the increasing number of patients who have cancer, the subsequent increase in the demand for cancer therapies and the growing R&D expenditure by pharmaceutical companies in this therapeutic area.

North America is expected to dominate the drug discovery services market in 2020.

North America, which includes the US and Canada, is estimated to account for the largest share of the drug discovery services market. The large share of this region can primarily be attributed to the presence of well-established CROs; rising R&D expenditure by pharmaceutical & biopharmaceutical companies and the availability of latest techniques, instruments, and facilities for drug discovery research are driving the growth of this region.

Reasons to Buy the Report:

Key Topics Covered:

1 Introduction

1.1 Objectives of the Study

1.2 Market Definition

1.3 Market Scope

1.4 Currency

1.5 Limitations

1.6 Stakeholders

2 Research Methodology

2.1 Research Data

2.2 Market Size Estimation

2.3 Market Breakdown and Data Triangulation

2.4 Assumptions for the Study

3 Executive Summary

4 Premium Insights

4.1 Drug Discovery Services Market Overview

4.2 North America: Market, By Drug Type & Country (2020)

4.3 Market: Geographic Growth Opportunities

5 Market Overview

5.1 Introduction

5.2 Market Dynamics

5.2.1 Drivers

5.2.2 Restraints

5.2.3 Opportunities

5.2.4 Trends

6 Drug Discovery Services Market, By Process

6.1 Introduction

6.2 Target Selection

6.3 Target Validation

6.4 Hit-To-Lead Identification

6.5 Lead Optimization

6.6 Candidate Validation

7 Drug Discovery Services Market, By Type

7.1 Introduction

7.2 Medicinal Chemistry Services

7.3 Biology Services

7.4 Drug Metabolism & Pharmacokinetics

8 Drug Discovery Services Market, By Drug Type

8.1 Introduction

8.2 Small-Molecule Drugs

8.3 Biologic Drugs

9 Drug Discovery Services Market, By Therapeutic Area

9.1 Introduction

9.2 Oncology

9.3 Neurology

9.4 Infectious and Immune System Diseases

9.5 Digestive System Diseases

9.6 Cardiovascular Diseases

9.7 Other Therapeutic Areas

10 Drug Discovery Services Market, By Company Type

10.1 Introduction

10.2 Tier 1 Pharmaceutical Companies

10.3 Tier 2 Pharmaceutical Companies

10.4 Tier 3 Pharmaceutical Companies

11 Drug Discovery Services Market, By Region

11.1 Introduction

11.2 North America

11.3 Europe

11.4 Asia Pacific

11.5 Rest of the World

12 Competitive Landscape

12.1 Overview

12.2 Market Share Analysis

12.3 Competitive Scenario

12.4 Competitive Leadership Mapping

13 Company Profiles

13.1 Laboratory Corporation of America Holdings

13.2 Eurofins Scientific Se

13.3 Charles River Laboratories International

13.4 Evotec SE

13.5 Thermo Fisher Scientific

13.6 Albany Molecular Research, Inc.

13.7 Syngene International Limited

13.8 Jubilant Lifesciences

13.9 Genscript Biotech Corporation

13.10 Piramal Enterprises Limited

13.11 Selvita S.A.

13.12 Aurigene Discovery Technologies

13.13 Domainex Ltd.

13.14 WuXi AppTec

13.15 Chempartner Co., Ltd.

13.16 Frontage Holdings

13.17 Pharmaceutical Product Development, LLC

13.18 Shanghai Medicilon, Inc.

13.19 TCG Lifesciences Pvt. Limited

13.20 Viva Biotech (Shanghai) Ltd.

For more information about this report visit https://www.researchandmarkets.com/r/i0k3fl

Originally posted here:
Global Drug Discovery Services Market is Projected to Reach USD 19.1 Billion By 2025 at a CAGR of 12.1% from 2020 to 2025 - ResearchAndMarkets.com -...

An 8.42% Dip in Hospitalizations and 7.83% Gain in Hospitalization via ER for Orthopedics at Yale New Haven Hospital, New Haven County

By: Avinash Kumar  Feb. 10, 2020

Dexur utilized Medicare claims data from 2014-Q2 to 2019-Q2 to analyze the market share of Yale New Haven Hospital of New Haven County on different metrics like Specialties, Conditions, DRG groups, Outpatient ER Visits, Hospitalizations via ER.

Yale New Haven Hospital of New Haven County maintained a consistent hospitalization rate at around 45% to 50% with 47.82% market share in 2014-Q2 and 48.65% in 2018-Q2, however when analyzed at the specialty level, there was a difference.

Orthopedics specialty of Yale New Haven Hospital, New Haven County, had seen a dip of 8.42% in hospitalizations from 2014 to 2018 with a market share of 46.61% in 2014 to 38.19% in 2018. However, based on the data analysis of 2018-Q2 to 2019-Q2, a decrease of 2.74% in the Orthopedic market share is observed. Other specialties that saw a decrease in market share are Neurology, Cardiovascular, Gastroenterology & Endocrinology, with a growth of 8.46%, 4.22%, and 4.16%, respectively, from 2014 to 2018.

Furthermore, Dexur also analyzed the share of hospitalizations admitted via ER. An increase of 6.86% in hospitalization rate via ED with 43.3% market share in 2014-Q2 and 50.16% in 2019-Q2 in New Haven County for Yale New Haven Hospital was recorded.

The Orthopedic specialty, which showed a decrease of 8.42% market share in hospitalizations, showed an increase of 7.83% in hospitalizations via ER.The market share of other specialties like Psychiatry & Mental Disorders, Neurology, and Cardiovascular increased by 8.58%, 8.12%, and 7.8% respectively from 2014 to 2018.

Continue reading here:
An 8.42% Dip in Hospitalizations and 7.83% Gain in Hospitalization via ER for Orthopedics at Yale New Haven Hospital, New Haven County - Dexur

People with neurological conditions like Parkinsons disease, multiple sclerosis (MS), amyotrophic lateral sclerosis (ALS, also known as Lou Gehrigs disease), Huntingtons disease, and dementia are at higher risk for suicide, a study published in February 2020 in the Journal of the American Medical Association has found.

According to the authors, from the Danish Research Institute for Suicide Prevention (DRISP) in Copenhagen, the higher rates of suicide among those with these brain disorders are likely the result of stress and feelings of hopelessness when they learn their diagnosis and prognosis. Although the symptoms of most of these conditions can be managed with drug treatments and other approaches, none can be cured at least not yet.

In addition, many of these disorders lead to significant disability, which may impact the quality of life of those who are diagnosed as well as their families and friends.

Distress at the time of diagnosis plays a role, for instance, for people with dementia, explains study coauthor Annette Erlangsen, PhD, who heads the research program at DRISP. For severe disorders, such as Huntingtons and ALS, the risk of suicide might be related to the course of the disorder.

Some of these disorders, perhaps as a result, are also linked with a higher risk of mood disorders like depression and anxiety, which may lead to thoughts of suicide, she adds.

To assess the risk of suicide among people with certain neurological disorders, Dr. Erlangsen and her colleagues reviewed the health records of more than 7.3 million people in Denmark from 1980 through 2016. All of the people included in the analysis were 15 years of age or older as of 1980, and approximately 1.25 million of them had received medical treatment for a head injury, stroke, epilepsy, polyneuropathy, diseases of myoneural junction (in which signals from nerves to muscles are disrupted, leading to muscle weakness and fatigue), Parkinsons, MS, central nervous system infections, meningitis, encephalitis, ALS, Huntingtons, dementia, intellectual disability, and other brain-related conditions during the study period.

Ultimately, more than 35,000 of those included in the analysis died by suicide, and nearly 15 percent of those who died by suicide had been diagnosed with a neurological disorder. Overall, Erlangsens team found that those with neurological disorders are almost twice as likely to take their own lives as those who hadnt been diagnosed with these conditions.

Risk of suicide among those with ALS was almost 5 times higher than that of the general population, while the suicide risk for those with Huntingtons, MS, and epilepsy was roughly twice as high.

The researchers also found that the risk of suicide rose as the number of hospital visits rose.

RELATED: What Your Doctor Wont Tell You About Epilepsy: It Can Kill You

Based on their findings, the authors suggest that caregivers friends and loved ones as well as healthcare professionals closely monitor those with these conditions for depression and anxiety, emotional distress, and suicidal thoughts.

Its important to emphasize that suicide is a rare event in general and also among people with neurological disorders, Erlangsen says. However, she adds, Its surely important to be aware of ones mental well-being especially when diagnosed with a chronic disorder. Luckily, its few who develop depressive symptoms, but if one does, then it is important to speak to a healthcare professional and assess whether further initiatives are needed.

More here:
Study Finds Suicide Rate Higher Among Those With Neurological Disorders - Everyday Health

Patients are benefiting from a new hospital ward opening up in Aberdeen.

Neurosurgery patients suffering from acute illness, such as brain injuries, have been sharing a space at Aberdeen Royal Infirmary with neurology patients with chronic or life-limiting conditions.

The two groups require different types of care and NHS Grampian has now launched a dedicated space for people admitted for neurology care.

Describing the layout before the change, consultant neurosurgeon Anastasios Giamouriadis said: We would have a patient who is recovering from surgery for a brain tumour and were expecting improvement nursed in a bed next to a patient with progressive motor neurone disease (MND) that we are trying to delay the worsening and deterioration of the neurological condition.

As far as the staff are concerned these patients have different needs. Whereby neurosurgery patients need less and less support neurology patients need more support over time.

Caroline McIntosh, who is the senior charge nurse for the new neurology ward also known as Ward 204 said: Its an opportunity to enhance the already excellent care we are giving patients.

Weve been working to specialities in one unit and doing it exceptionally well with lots of positive feedback.

Claire McNab, senior charge nurse for the neurosurgery ward known as Ward 205 said: This is an evolution of the service we already offer to further improve the care we provide.

The way you nurse both sets of patients is very different.

Neurosurgical patients come in either for a listed operative procedure or with an acute illness where they receive surgery and then either go on to receive oncology services or rehab.

They are with us for their neuro treatment be it brain surgery, spinal or something similar and then they tend to go on for specialist care in different areas.

With neurology patients, because they usually have a life-limiting or chronic illness, like MS or MND, the management of that is quite different.

Ward 204 will have 10 beds and Ward 205 will have 17 beds maintaining the same number as before the change.

Caroline said she hoped having two dedicated wards will help attract graduate nurses in both neurology and neurosurgery.

She added: It will provide a better environment for learning for newly qualified nurses and we will hopefully capture their interest in one area and can go on to further their education and training from there.

Hopefully over the next five years we will see benefits and staff vacancies will drop as a result and it will help us recruit new people and also retain them.

Although we are going to be two separate wards it will still be a neuroscience floor and we will work together for the best of the patients.

On the same floor is the neurophysiology department and we also have the planned investigation unit.

Read more from the original source:
New Aberdeen hospital ward gives neurology patients the care they need - Aberdeen Evening Express

What Is the GutBrain Axis?

Intestinal health is quickly becoming one of the most critical components in maintaining optimal well-being, including mental/emotional as well as physical. In recent years, it has become more common to refer to the gut as our second brain, meaning it can engage in neurological activity independently from the central nervous system. At any given moment, the brain and the gut are in complex, essential communication, giving rise to a two-way flow of information called the gutbrain axis.

The second brainin technical parlance, the enteric nervous system (ENS)controls the gastrointestinal (GI) system and is linked to the brain by millions of neurons. While our ENS is in constant contact with the central nervous system, it can also act independently, performing the important role of monitoring the entire digestive tract without direct supervision from the brain.

The ENS is made up of two thin layers with more than 100 million neurons in themmore than the spinal cord. These cells line the gastrointestinal tract, controlling blood flow and secretions to help the GI tract digest food. They also help us feel whats happening inside the gut, since this second brain is behind the mechanics of food digestion.

While the second brain doesnt get involved in thought processes like political debates or theological reflection, it does control behavior on its own. Researchers believe this came about to make digestion more efficient in the body; instead of having to direct digestion through the spinal cord and into the brain and back, we developed an on-site brain that could handle things closer to the source.

The gut and brain are also connected through chemicals called neurotransmitters. Those produced in the brain control feelings and emotions. The best known of these is serotonin, which contributes to feelings of well-being. Another very important one is gamma-aminobutyric acid (GABA), which helps control feelings of fear and anxiety and helps with sleep regulation. A large proportion of serotonin, GABA, and other neurotransmitters are produced by gut cells and the trillions of microbes living in the GI tract.

It used to be thought that neurological disorders such as depression and anxiety trigger autoimmune conditions such as irritable bowel syndrome or other digestive-related issues. However, the opposite is likely truein other words, dysfunction in the gut may in fact cause changes in mood and behavior, triggered by the enteric nervous system. An estimated 30 to 40 percent of the population suffers from digestive-related illness, which helps explain why a higher-than-normal percentage of people with a compromised gut suffer from mood-related challenges such as depression and anxiety.

As our understanding of the gutbrain axis deepens, we are gaining a better appreciation for why taking good care of our gastrointestinal health can lead to significant improvements in our mental and emotional well-being.

What Can Disrupt the GutBrain Connection?

Stress has very deleterious effects on health, including the gutbrain axis. Our bodys immediate reaction to stress, whether physical or mental, is to release the hormone adrenaline and other stress hormones to help us survive. For instance, if youre hiking and encounter a mountain lion, your body goes into survival mode. Your heart beats faster, your eyes widen, and even your blood platelets become sticky in case the dangerous encounter leaves you bleeding; your blood will clot more quickly. Once the stressful situation is over, your body stands down from the fight-or-flight response and returns to normal.

This is perfectly healthy. The problem arises when youre living in a chronic state of stressworking in a stressful environment, for example. Since your body cannot differentiate between a physical stressor, like being pursued by a mountain lion, versus a mental stressor, like an unpleasant job, it reacts the same way and keeps on reacting. The prolonged presence of adrenaline and other stress-related hormones generates inflammation throughout your body.

Inflammation is the immune systems natural response to toxins, infection, and stress. If inflammation is experienced over a prolonged period of time, the immune system weakens, leading to neurodegenerative diseases such as Alzheimers and Parkinsons, as well as neurological disorders such as ADHD, autism, anxiety, and depression. Roughly 80 percent of the immune system is located in the gut, which makes gut health a primary concern to achieve optimal health.

Environmental toxins are substances that work in direct opposition to natural healing and can have a very negative effect on the gutbrain connection; they are numerous and include lead, mercury, cadmium, and arsenic. Environmental toxins can create a negative and potentially life-altering pattern in the brain and body (the brainbody) or worsen a negative pattern. They tell your brain to stop healing the body, and they can make you jittery and reactive.

We carry these toxins in our fat tissues and release them with fat loss. Most of us also carry the most common environmental toxins in our bones, and every daythrough our diet, the water we drink, the products we usewe take in a little more. Around age thirty-five, as bone buildup slows down and bone breakdown begins, the body slowly releases these substances into the bloodstream. The brainbody can become a little more poisoned each day from this internal storehouse of toxic substances, as well as new exposures, including in the food we eatespecially foods with pesticides, herbicides, genetically engineered ingredients, and hormonesthe water we drink, the products we use, and the air we breathe.

Glyphosate is a weapon of mass destruction in our food supply that is ruining the gutbrain connection. It disrupts the integrity of the gut barrier and may then disrupt the integrity of the bloodbrain barrier, leading to inflammation. Glyphosate is associated with increased anxiety, attention deficit, depression, weight gain, cancer, memory impairment, and other brainbody problems. Its residues are commonly found in GMO foods and conventional wine.

The Role of Microbes in the GutBrain Axis

Gut health is determined by the collection of bacteria that resides in the GI tract, commonly referred to as the microbiome. The key to optimal gut health is maintaining a healthy diversity and balance of good and bad bacteria in the microbiome.

The microbiome plays a crucial role in the immune system and in brain function. The overgrowth of bad bacteria can cause many complications, such as dysbiosis (microbial imbalance) and bacterial overgrowth in the gut. These eventually lead to more serious conditions, including inflammatory bowel diseases such as Crohns disease and ulcerative colitis, as well as neurological issues such as depression and anxiety.

The trillions of microbes in the gut make numerous chemicals that affect the brain. Certain gut bacteria make a compound called brain-derived neurotropic factor, which helps the brain stay young and build new pathways. A healthy brain requires the right level of hormones to stay sharp, and the right neurotransmitters to focus, and the microbiome makes vital contributions in both respects. Gut microbes also produce abundant short-chain fatty acids (SCFAs), such as butyrate, propionate, and acetate, by digesting fiber. SCFAs affect brain function in a number of ways, such as by reducing appetite. Finally, gut microbes metabolize bile acids and amino acids to produce other chemicals that affect the brain.

As such a large proportion of the immune system is located in the gut, the microbiome plays a key role in that systems functioning by controlling what is passed into the body and what is excreted. When the microbiome isnt healthy, inflammation results, which is associated with a number of brain disorders, including depression, anxiety, Alzheimers, dementia, and schizophrenia.

Clearly, if we want to repair breakdowns in the gutbrain axis, we need to focus on the microbiome. There is now extensive research being executed to explore how the microbiome can be utilized to fight illness and disease.

Ways to Repair the GutBrain Connection

Probioticsare supplements containing specific strains of bacteria that contribute to maintaining a healthy microbiome in the gut. Studies show that taking probiotics can reduce feelings of depression and anxiety and improved overall well-being.

A recent study looked at how the gut and brain are connected by examining the effects of probiotics on patients with irritable bowel syndrome and depression. The researchers found that twice as many patients saw improvements from depression when they took the probiotic Bifidobacterium longum NCC3001 daily compared with patients who took a placebo. Studies in laboratory mice have shown that certain probiotics can increase the production of GABA and reduce anxiety and depression-like behavior.

Fermented foods contain various species of Lactobacillus and Bifidobacterium bacteria that can contribute positively to the microbiome. Examples include sauerkraut, kimchi, and kefir.

The good bacteria in the guts microbiome require appropriate food materials, and these are known asprebiotics. The best sources for prebiotics are: asparagus, bananas, carrots, chicory root, coconut meat & flour, dandelion greens, flax and chia seeds, garlic, Jerusalem artichoke, jicama, leeks, onions, radishes, tomatoes, yams.

Bone broth is one of the most healing and nourishing foods for the gut. It aids in reducing inflammation and helps provide the gut with the necessary nutrients for healing. Bone broth also contains collagen and cartilage, two proteins that help rebuild the gut lining, as well as glycine, proline, and l-glutamineamino acids that are essential for repairing and rebuilding the body. L-glutamine promotes digestive health, brain function, and muscle integrity. It is an important nutrient in relation to the gut, because it helps repair and rebuild intestines and strengthen the gut lining.

You can also use your beliefs along with the basics of neuroscience to improve spiritual neuroplasticity and build a better, healthier brain-body connection. Something as simple as awalking meditation on a daily basis can lead to important changes. A daily practice can increase blood flow to the brain, grow the grey matter and create a connection to something greater. This has measurable effects on the brain that improve brain-body physiology and provide a shield against the normal stress of daily life.

Although the brain represents only 23 percent of the bodys total weight, it consumes 25 percent of the bodys glucose supply and 20 percent of its oxygen and cardiac output. The brain is the single biggest consumer of what we put into our bodies, yet most of us dont consider our brains when making food choices, focusing instead on calories. We rarely think of how our brain is going to benefit or suffer from our food choices.

In reality, the food you consume has the potential to help or hurt your gut first, then your brain, and finally the rest of your body. Food is information not only for the DNA of your cells but also for the DNA of the microbes in your gut. The food on your fork determines your gene expression, hormone levels, immune activityeven the stress levels in your gut, your brain, and the rest of your body. A change in the food you eat rapidly alters the activity of the gut microbiotatypically within one to four days, and in some cases, within just six hours.

A healthy brainbody connection exists when your brain and your body are fully in sync and congruent in their mission and goals. Healing conversations are occurring. Your gut is having a healing conversation with your brain, and your heart is telling your brains overactive stress-response system that it can calm down. In short, having a healthy brainbody connection means that you dont have the high levels of inflammation that cause brainbody breakdown.

Visit link:
The GutBrain Connection: - Thrive Global