More than 10 million people worldwideabout 1 percent of people over age 60live with Parkinsons disease. There are treatments that can help control symptoms, but there is no cure.

The hallmark of the disease is the death of certain brain cellsneurons that produce dopamine. Most Parkinsons researchers have focused on studying these cells. But what if the disease starts elsewhere? What if it involves not only neurons but other cells that interact with neurons? In particular, what role is played by astrocytes, star-shaped cells that nurture and help form the connections, or synapses, between the neurons?

(This article by Angela Spivey, with photos by Alex Boerner, originally appeared in Duke Medical Alumni News. Read that story here.)

Thats the question a team of Duke researchers led by Cagla Eroglu, PhD, associate professor of cell biology and neurobiology, is exploring, thanks to a $1 million grant from the Chan Zuckerberg Initiative.

Sitting in her office, Eroglu picks up an orange plastic object that resembles a piece of coral, its tentacles branching this way and that. This is a model of a mouse astrocyte, she says. It can interact with 100,000 synapses at the same time. Astrocytes, she explains, infiltrate the brain, touching everything within their reach. They communicate with its synapses, regulating blood flow and metabolism.

Astrocytes from the Greek astron, meaning "star"have traditionally been thought of as support cells. But that thinking is changing. Since astrocytes are in such close contact and continuously communicating with synapses, we are beginning to appreciate that they are also fundamentally involved in regulating brain function, Eroglu says.

Collaborating with Albert La Spada, MD, PhD, Eroglu found that a certain gene known to be important in Parkinsons is more highly expressed in astrocytes than in neurons. And when the researchers mutated that gene in astrocytes, they saw some intriguing changes. This still-unpublished work laid the foundation for their proposal to the Chan Zuckerberg Initiative, which is bringing together experimental scientists from divergent fields to take a fresh look at the causes of neurodegenerative disorders.

There are vanishingly few papers that have delved into how astrocytes are contributing to the Parkinsons disease process, says La Spada, professor of neurology and vice chair of research for the Department of Neurology. This is an area that's been under-studied, and I think that the results that we're generating are suggesting that it deserves more attention.In addition to his long experience studying neurodegenerative diseases, La Spada brings expertise in growing astrocytes from induced pluripotent stem cells (IPSCs). That process starts by growing skin cells from a skin biopsy from a Parkinsons patient. Then we use what's called a reprogramming protocol to basically revert them to stem cells that are pluripotent. Once you create the IPSCs, you could use them to make any cell you wanta muscle cell or a cardiac cell or a neuron or an astrocyte, La Spada says. The beauty of this is, it comes from the patient who has the disease of interest."

His labs expertise will only grow because of the Chan Zuckerberg Initiative, which has formed focus groups for grantees around various areas, such as stem cell modeling, CRISPR gene-editing technology, bioinformatic analysis of data sets, and more. We're meeting other researchers from around the world who are doing really unique things. It's a chance for us all to compare notes, and I think this will accelerate all of our endeavors, La Spada says.

Rounding out the team is Nicole Calakos, MD, PhD, a scientist and clinician who treats patients with movement disorders, including Parkinsons. Calakos says that when she first met Eroglu, she was intrigued by her idea that since astrocytes are involved in sculpting the language of neurons, perhaps they play a role in the events that can lead to disease.

Everybody has been fixated like a magnet on the idea that the problem is the neuron that's dying, Calakos says. Cagla said, Hey, let's think outside of the box of that dead cell. Lets consider whether astrocytes are like the soil around a plant, providing the nutrition, and allowing it to form roots, and maybe that is whats broken. Why aren't we even thinking about this critical piece of the brain?

Eroglu puts it this way: Maybe the problem is loss of connections between neurons, even before they die.

Calakos says that part of the reason she came to Duke was the close intermingling of physicians and bench scientists. Because of how the community is at Duke, Cagla and I had been exchanging ideas and collaborating over the years, she says. The Chan Zuckerberg grant is an opportunity to get together as a formal team. I think it's really forward-thinking of them to have teams of basic scientists and practicing physicians all talking to each other.

The Chan Zuckerberg Initiative was launched in December 2015 by Mark Zuckerberg, founder and CEO of Facebook, and Priscilla Chan, a pediatrician and founder and CEO of The Primary School in East Palo Alto. In addition to her clinical insight, Calakos brings expertise in electrophysiologyreal-time recording and observation of electrical signals coming from brain cells. We can listen to the language of synapses, she says. They speak in electrical currents,which we can measure. Eroglu believes that by learning all they can about how astrocytes support synaptic development and health in the normal brain, they may find ways to stop neurodegenerative diseases like Parkinsons.

We are seeing aging as a part of development, Eroglu says. If your house is built on a strong base, then it might last longer. Whereas, if you build it in another way, it may be there for a while, but gradually start to break down.

This doesn't mean that we are destined to have neurodegeneration and we can't do anything. We may be more predisposed to get the disease, but we may not get it if we have done something else in our lives that helps strengthen our brain. I strongly believe that there will be ways to stop neurodegeneration.We will find a way to strengthen the brain connections. If we can figure out the weakest link, then we could concentrate on solving that.

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The Stars in Our Brains - Duke Department of Neurology

This transcript has been edited for clarity.

Dear colleagues, I am Christoph Diener, a neurologist from the University of Duisburg-Essen in Germany. Today I would like to discuss six noteworthy publications that came out in September of this year.

The EPIC-Oxford study recruited 48,000 people without stroke or ischemic heart disease and followed them for 20 years. Participants were divided into three groups: meat eaters, fish- but not meat eaters, and vegetarians.

Researchers published the results of 18 years of follow-up of these participants in the BMJ,[1] reporting 2820 cases of ischemic heart disease and 1072 cases of stroke during that time. Compared with meat eaters, fish eaters and vegetarians had a 13% and 22% relative risk reduction of developing ischemic heart disease, respectively. In absolute numbers, this accounts for 10 fewer cases of heart disease per 1000 for vegetarians compared with meat eaters over 10 years. Interestingly, and surprisingly, vegetarians had a 20% higher risk for stroke than meat eaters, mostly due to cerebral hemorrhage. In absolute numbers, this accounts for three more cases out of 1000 over 10 years.

I think the most likely explanation for why meat eaters have a higher risk for ischemic heart disease is LDL cholesterol. This could also explain the increased risk for cerebral hemorrhage, as it's known that very low LDL can [be associated with] a slightly higher risk for stroke.

The European Stroke Organisation offered guidelines on antithrombotic therapy for secondary stroke prevention in patients with atrial fibrillation in the European Stroke Journal.[2]

The most important recommendation is that antiplatelet therapy should no longer be used. The second recommendation is that vitamin K antagonists should be used compared with no treatment or with aspirin, and nonvitamin K antagonist oral anticoagulants are preferred over vitamin K antagonists. There is no recommendation about the timing of when to initiate treatment after ischemic stroke. Another important recommendation is that no bridging with low-molecular-weight heparin is needed until anticoagulation is started. At the moment, there is no recommendation on occlusion of the left atrial appendage in patients with contraindications for long-term anticoagulation, given that the ongoing trials are not yet finished.

A third, very interesting paper was published in Lancet Neurology,[3] looking at people with cerebral cavernous malformations. Investigators identified 300 patients in a registry and followed them for 7 years to determine whether antithrombotic therapy or anticoagulation had an impact on the risk for intracerebral bleeding. Approximately 20% of patients were on antiplatelet therapy or anticoagulation, and they clearly had a lower risk for intracranial hemorrhage. They also performed a meta-analysis of six cohort studies with 1342 patients, which basically showed the same result: a reduced risk for intracerebral hemorrhage with antithrombotic therapy.

The most likely explanation for these results is that antithrombotic therapy allows you to avoid venous thrombosis that can lead to hemorrhage.

We recently published the results of the RE-SPECT CVT Study in JAMA Neurology.[4] This was a safety study in 100 patients with cerebral venous thrombosis, who were randomized to either high-dose dabigatran (150 mg twice daily) or warfarin for 25 weeks after an initial treatment period of low-molecular-weight heparin. There was one intestinal bleed on the dabigatran, two intracranial bleeds on warfarin, and no recurrent venous events.

The good news here is that dabigatran is as safe as warfarin for the prevention of recurrent venous events in cerebral venous thrombosis. However, the drug is not approved for this indication.

In a study published in Annals of Neurology,[5] 140 patients with epilepsy and current major depressive disorder were randomized to receive sertraline or cognitive-behavioral therapy for 16 weeks. Both treatments were effective, with over 50% of patients achieving remission. Importantly, sertraline does not increase the risk for seizures.

Ideally, I think these two treatment methods should be combined in such patients.

The last study dealt with Duchenne muscular dystrophy and was published in Neurology.[6] Young boys with this disorder are usually treated with prednisone, with all of the adverse events that this entails when given long-term.

There is now a new drug called vamorolone which has similar activity to prednisone, but it doesn't have the side effects. In this dose-finding study, vamorolone at 2 mg/day improved motor function and clearly had fewer adverse events than the historical controls of prednisone or cortisone. We now need phase 3 trials to show whether this effect is also replicated in everyday clinical practice.

Ladies and gentlemen, we have six new studies of interest: four on stroke, one on depression and epilepsy, and one on Duchenne muscular dystrophy. Thank you very much for watching and listening.

Hans-Christoph Diener, MD, PhD, is a professor in the Department of Neurology at University Duisburg-Essen in Essen, Germany. He is widely published and best known for his contributions to stroke and headache medicine.

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Meat, Fish, and Vegetables: New Data on Heart Disease and Stroke - Medscape

Most of the time when we think about genetic mutations, we think about the ones that spell disaster. But sometimes, our genes can have the opposite effect: Instead of increasing our risk for certain diseases, they can protect us from them.

This has turned out to be the case with a Colombian woman in her 70s. By all indications, she shouldhave developed Alzheimers disease by her mid-40s. She has one of three rare mutations that lead to early-onset Alzheimers diseasepeople with this mutation only make up about 1% the 44 million individuals living with Alzheimers globally. And yet, by the time she turned 70 she was still mostly healthy; although she has developed mild cognitive impairment, which can be a warning sign for Alzheimers, she may never experience dementia.

The reason for her continued health? A super rare mutation to both copies of anothergene related to Alzheimers, called APOE. Called the Christchurch mutation (for the town in New Zealand where scientists discovered it in the 1980s), it seems to somehow counteract the risk of Alzheimers diseaseand could inspire future treatments or preventions for it. Researchers in the US and in Colombia published the womans case study on Monday, Nov. 4 in the journal Nature Medicine.

The woman, who is still alive and living in Colombia, comes from a family where dominantly-inherited Alzheimers is common. She and some 6,000 members of her kindred participate in the Colombia Alzheimers Prevention Registry, which is run by Francisco Lopera, a neurologist at the University of Antioquia in Colombia. Some 1,200 people in the registry have a mutation that causes them to over-produce amyloid protein in the brain, one of the hallmark signs of the disease. Everyone in the registry can enroll in clinical research trials for Alzheimers.

This particular woman, however, never got sick. When researchers maintaining the registry noticed that it took her three decades to even develop mild cognitive impairment, they flew her to Boston, where she agreed to let researchers at Harvard University conduct a series of tests.

What they found in her brain imaging shocked them. She had the highest amyloid beta burden of anyone else in the cohort, says Eric Reiman, a neurologist with the Banner Alzheimers Institute in Arizona, who co-authored the paper. This was consistent with her dominantly-inherited Alzheimers mutation. Normally, these high levels of amyloid are thought to lead to buildups of another deformed protein, called tau, along with inflammation and the ultimate destruction of neurons.

But the woman didnt have the characteristic tangles of tau. And the regions of her brain that are most commonly affected by Alzheimers still seemed to be working just like they would in an otherwise healthy adult.

When they sequenced her whole genome, researchers found that her APOE gene had two copies of the Christchurch mutation: a single basepair switch that tweaks the protein produced by the gene. Somehow, this tweaked version of the protein seemed to mitigate the effects of the extra amyloid in her brain.

That means targeting these downstream effects, in addition to amyloid itself, may be a viable treatment for Alzheimersalthough its not clear how to go about that just yet. The vast majority of drug trials targeting amyloid have failed, with the notable exception of one trial from the drug company Biogen that appears to have had positive results. Having more targets increases the likelihood of having more successful treatments that work for more people, or even combination therapies.

This case study leads us to think about the importance of such studies in relatively understudied populations, says Nilufer Ertekin-Taner, a neurogeneticist with the Mayo Clinic in Jacksonville, Florida, who was not involved with the study. Scientific knowledge of the Christchurch mutation suggests that its incredibly rare, but that could be because the majority of research on Alzheimers and dementia has been done on white populations. By including more diverse populations in future research, scientists can get a better idea of how this mutation works in other healthy populationsand ultimately, how it could mitigate the disease overall.

Correction (Nov. 4): An earlier version of this story accidentally mis-named Eric Reiman as Dan Reiman.

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Rare genetic mutations protected a woman from developing Alzheimer's - Quartz

The womans genetic profile showed she would develop Alzheimers by the time she turned 50.

A member of the worlds largest family to suffer from Alzheimers, she, like generations of her relatives, was born with a gene mutation that causes people to begin having memory and thinking problems in their 40s and deteriorate rapidly toward death around age 60.

But remarkably, she experienced no cognitive decline at all until her 70s, nearly three decades later than expected.

How did that happen? New research provides an answer, one that experts say could change the scientific understanding of Alzheimers disease and inspire new ideas about how to prevent and treat it.

In a study published Monday in the journal Nature Medicine, researchers say the woman, whose name they withheld to protect her privacy, has another mutation that has protected her from dementia even though her brain has developed a major neurological feature of Alzheimers disease.

This ultra rare mutation appears to help stave off the disease by minimizing the binding of a particular sugar compound to an important gene. That finding suggests that treatments could be developed to give other people that same protective mechanism.

Im very excited to see this new study come out the impact is dramatic, said Dr. Yadong Huang, a senior investigator at Gladstone Institutes, who was not involved in the research. For both research and therapeutic development, this new finding is very important.

A drug or gene therapy would not be available any time soon because scientists first need to replicate the protective mechanism found in this one patient by testing it in laboratory animals and human brain cells.

Still, this case comes at a time when the Alzheimers field is craving new approaches after billions of dollars has been spent on developing and testing treatments and some 200 drug trials have failed. It has been more than 15 years since the last treatment for dementia was approved, and the few drugs available do not work very well for very long.

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The woman is entering her late 70s now and lives in Medelln, the epicenter for an extended Colombian family of about 6,000 people whose members have been plagued with dementia for centuries, a condition they called La Bobera - the foolishness - and attributed to superstitious causes.

Decades ago, a Colombian neurologist, Dr. Francisco Lopera, began painstakingly collecting the familys birth and death records in Medelln and remote Andes mountain villages. He documented the sprawling family tree and took dangerous risks in guerrilla and drug-trafficking territory to cajole relatives of people who died with dementia into giving him their brains for analysis.

Through this work, Dr. Lopera, whose brain bank at the University of Antioquia now contains 300 brains, helped discover that their Alzheimers was caused by a mutation on a gene called Presenilin 1.

While this type of hereditary early-onset dementia accounts for only a small proportion of the roughly 30 million people worldwide with Alzheimers, it is important because unlike most forms of Alzheimers, the Colombian version has been traced to a specific cause and a consistent pattern. So Dr. Lopera and a team of American scientists have spent years studying the family, searching for answers both to help the Colombians and to address the mounting epidemic of the more typical old-age Alzheimers disease.

When they found that the woman had the Presenilin 1 mutation, but had not yet even developed a pre-Alzheimers condition called mild cognitive impairment, the scientists were mystified.

We have a single person who is resilient to Alzheimers disease when she should be at high risk, said Dr. Eric Reiman, executive director of the Banner Alzheimers Institute in Phoenix and a leader of the research team.

The woman was flown to Boston, where some of the researchers are based, for brain scans and other tests. Those results were puzzling, said Yakeel Quiroz, a Colombian neuropsychologist who directs the familial dementia neuroimaging lab at Massachusetts General Hospital.

The womans brain was laden with the foremost hallmark of Alzheimers: plaques of amyloid protein.

The highest levels of amyloid that we have seen so far, said Dr. Quiroz, adding that the excessive amyloid probably accumulated because the woman has lived much longer than other family members with the Alzheimers-causing mutation.

But the woman had few other neurological signs of the disease not much of a protein called tau, which forms tangles in Alzheimers brains, and little neurodegeneration or brain atrophy.

Her brain was functioning really well, said Dr. Quiroz, who, like Dr. Reiman, is a senior author of the study. Compared to people who are 45 or 50, shes actually better.

She said the woman, who raised four children, had only one year of formal education and could barely read or write, so it was unlikely her cognitive protection came from educational stimulation.

She has a secret in her biology, Dr. Lopera said. This case is a big window to discover new approaches.

Dr. Quiroz consulted Dr. Joseph Arboleda-Velasquez, who, like her, is an assistant professor at Harvard Medical School (he is also Dr. Quirozs husband). Dr. Arboleda-Velasquez, a cell biologist at Massachusetts Eye and Ear, conducted extensive genetic testing and sequencing, determining that the woman has an extremely rare mutation on a gene called APOE.

APOE is important in general-population Alzheimers. One variant, APOE4, present in about 14 percent of people, greatly increases risk and is present in 40 percent of people with Alzheimers. People with another variant, APOE2, occurring in about 7 percent of the population, are less likely to develop Alzheimers, while those with the most common variant, APOE3, are in the middle.

The Colombian woman has two copies of APOE3, but both copies have a mutation called Christchurch (for the New Zealand city where it was discovered). The Christchurch mutation is extremely rare, but several years ago, Dr. Reimans daughter Rebecca, a technologist, helped determine that a handful of Colombian family members have that mutation on one of their APOE genes. They developed Alzheimers as early as their relatives, though unlike the woman with mutations on both APOE genes.

The fact that she had two copies, not just one, really kind of sealed the deal, Dr. Arboleda-Velasquez said.

The womans mutation is in an area of the APOE gene that binds with a sugar-protein compound called heparan sulfate proteoglycans (HSPG), which is involved in spreading tau in Alzheimers disease.

In laboratory experiments, the researchers found that the less a variant of APOE binds to HSPG, the less it is linked to Alzheimers. With the Christchurch mutation, there was barely any binding.

That, said Dr. Arboleda-Velasquez, was the piece that completed the puzzle because, Oh, this is how the mutation has such a strong effect.

Researchers were also able to develop a compound that, in laboratory dish experiments, mimicked the action of the mutation, suggesting its possible to make drugs that prevent APOE from binding to HSPG.

Dr. Guojun Bu, who studies APOE, said that while the findings involved a single case and more research is needed, the implications could be profound.

When you have delayed onset of Alzheimers by three decades, you say wow, said Dr. Bu, chairman of the neuroscience department at the Mayo Clinic in Jacksonville, Fla., who was not involved in the study.

He said the research suggests that instead of drugs attacking amyloid or tau, which have failed in many clinical trials, a medication or gene therapy targeting APOE could be promising.

Dr. Reiman, who led another newly published study showing that APOE has a bigger effect on a persons risk of getting Alzheimers than previously thought, said potential treatments could try to reduce or even silence APOE activity in the brain. People born without APOE appear to have no cognitive problems, but they do have very high cholesterol that requires treatment.

Dr. Huang, who wrote a commentary about the study and is affiliated with two companies focusing on potential APOE-related treatments, said the findings also challenge a leading Alzheimers theory about the role of amyloid.

Since the woman had huge amounts of amyloid but few other Alzheimers indicators, it actually illustrates, to my knowledge for the first time, a very clear dissociation of amyloid accumulation from tau pathology, neurodegeneration and even cognitive decline, he said.

Dr. Lopera said the woman is just beginning to develop dementia, and he recently disclosed her genetic profile to her four adult children, who each have only one copy of the Christchurch mutation.

The researchers are also evaluating a few other members of the Colombian family, who appear to also have some resistance to Alzheimers. They are not as old as the woman, and they do not have the Christchurch mutation, but the team hopes to find other genetic factors from studying them and examine whether those factors operate along the same or different biological pathways, Dr. Reiman said.

Weve learned that at least one individual can live for very long having the cause of Alzheimers, and shes resistant to it, Dr. Arboleda-Velasquez said. What this patient is teaching is there could be a pathway for correcting the disease.

Originally posted here:
Why Didnt She Get Alzheimers? The Answer Could Hold a Key to Fighting the Disease - The New York Times

DUBLIN--(BUSINESS WIRE)--The "Europe Pacemakers Market to 2027 - Regional Analysis and Forecasts By Product Type By Technology, By End User, and Country" report has been added to ResearchAndMarkets.com's offering.

The Europe pacemaker market is expected to reach US$ 2,408.5 Mn in 2027 from US$ 1,248.7 Mn in 2018. The market is projected to grow with a CAGR of 7.7% from 2019-2027.

Electronic implants are playing a pioneering role that helps to detect specific medical parameters. Additionally, these implants are able to take immediately autonomous therapeutic measures, combining diagnosis and treatment in a single system. The electronic medical implant is an emerging field in the medical industry and has led to various developments of the products, in the field of cardiology, neurology, and otology. Many of the market players are developing novel products in order to minimize the burden of cardiovascular diseases, neurological disorders, and hearing disorders.

For instance, in November 2017, Medtronic launched Azure pacemakers with BlueSync technology that increases the life of the pacemakers, thus reducing the number of device replacements. It also enables to secure and automatic wireless data transmission to physicians. Similarly, in July 2016, BIOTRONIK headquartered in Germany received CE approval for its new Edora pacemakers and cardiac resynchronization therapy pacemakers (CRT-Ps).

Moreover, the presence of pacemaker manufacturers in the European region is also likely to influence the pacemaker market in the European region. Osypka Medical GmbH, Cardiac Impulse S.R.L., Sorin Biomedica C.R.M., S.R.L. are manufacturers located in Europe.

In 2018, Europe pacemaker market held a market share of 22.8% of the global pacemaker market. The implantable pacemakers segment expected to dominate its market share and was valued at US$ 855.5 Mn in 2018 and is anticipated to reach US$ 1,687.2 Mn by 2027. On the other hand, implantable pacemakers segment is also anticipated to witness the fastest growth rate of 8.0% during the forecast period, 2019 to 2027.

Similarly, in 2018 single-chambered pacemaker segment by technology was valued at US$ 890.2 Mn in 2018 and is anticipated to reach US$ 1,736.8 Mn by 2027 and is also expected to grow at the fastest growth rate of 7.9% during the forecast period.

Furthermore, the hospitals & clinics segment held the largest market share of is also anticipated to witness the fastest growth rate of 8.0% during the forecast period, 2019 to 2027. This segment is also expected to dominate the market in 2027 as it is the primary care center for most of the population.

Key Topics Covered:

1. Introduction

1.1 Scope Of The Study

1.2 Research Report Guidance

2. Europe Pacemakers Market - Key Takeaways

3. Europe Pacemakers Market - Market Landscape

3.1 Overview

3.2 Market Segmentation

3.3 Pest Analysis

4. Europe Pacemakers Market- Key Market Dynamics

4.1 Key Market Drivers

4.1.1 Increasing Number Of New Cases of Cardiovascular Diseases (CVD) in Europe

4.1.2 Rapid Technological Advancements in Europe

4.2 Key Market Restraints

4.2.1 Faulty Pacemaker Raises Concerns Over Implantation

4.3 Key Market Opportunities

4.3.1 Growing Medical Technology Industry The European Region

4.4 Future Trends

4.4.1 The Leadless Pacemaker is a New Era In Cardiac Pacing

4.5 Impact analysis

5. Pacemakers Market - Europe Analysis

5.1 Europe Pacemakers Market Revenue Forecasts And Analysis

5.2 Market Positioning

5.3 Performance Of Key Players

6. Pacemakers Market - Europe Regulatory Scenario

7. Europe Pacemakers Market Analysis - By Product Type

7.1 Overview

7.2 Europe Pacemakers Market, By Product Type, 2018 & 2027 (%)

7.3 Europe Pacemakers Market Revenue And Forecasts To 2027, By Product Type (Us$ Mn)

7.4 Implantable Pacemakers Market

7.5 External Pacemakers Market

8. Europe Pacemakers Market Analysis - By Technology

8.1 Overview

8.2 Europe Pacemakers Market, By Technology, 2018 & 2027 (%)

8.3 Europe Pacemakers Market Revenue And Forecasts To 2027, By Technology (Us$ Mn)

8.4 Single Chambered Market

8.5 Dual Chambered Market

8.6 Bi-Ventricular Market

9. Europe Pacemakers Market Analysis - By End User

9.1 Overview

9.2 Europe Pacemakers Market, By End User, 2018 & 2027 (%)

9.3 Europe Pacemakers Market Revenue And Forecasts To 2027, By End User (Us$ Mn)

9.4 Hospitals Market

9.5 Ambulatory Surgical Centres Market

9.6 Others Market

10. Europe Pacemakers market

11. Pacemakers Market - Industry Landscape

11.1 Overview

11.2 Comparative Company Analysis

11.3 Growth Strategies Done By The Companies In The Market, (%)

11.4 Organic Developments

11.5 Inorganic Developments

12. Pacemakers Market-Key Company Profiles

For more information about this report visit https://www.researchandmarkets.com/r/gwns81

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Europe Pacemakers Market to 2027 - Regional Analysis and Forecasts By Product Type, Technology, End User, and Country - ResearchAndMarkets.com -...

While a lot more people are shifting to plant-based diets so as to achieve positive health results, they might not be reaping the benefits to the fullest as it is found that not all plants can do good to you.

In a new study, researchers have found that all plants arent good especially for the undernourished or people who depend on a single plant diet.

They also cautioned that growing interest in wild edibles raises the risk for people in wealthy countries, too, especially as some plants may become more toxic with changing climate, according to the findings published in the journal Environmental Neurology.

The bottom line is that plants and fungi were not put here for our benefit - they need to defend themselves, said Peter Spencer, professor of neurology in the OHSU School of Medicine and an affiliated faculty member of the Oregon Institute of Occupational Health Sciences at OHSU.

In the study, researchers catalogued a quartet of plants that sicken or kill undernourished people around the globe. The adverse neurological effects of food dependency on plant components with toxic potential constitute a significant global health issue, explained researchers.

Those in the list of the researchers include the potential neurotoxic effects of fruit of the ackee tree, an evergreen native to West Africa and favorite of Jamaica; lychee fruit, a delicious tropical fruit from southern Asia now eaten worldwide; grasspea, a protein-rich legume eaten on the Indian continent and the Horn of Africa; and cassava, a plant whose roots and leaves are consumed in across sub-Sahara.

Researchers elucidate ways in which they can rapidly and fatally affect brain function or, in the case of cassava and grasspea, gradually induce crippling disease.

This depends on the amount of plant product consumed along with the poor health of the people eating it; and the relative availability of each of these plants due to poverty, hunger and, increasingly, climate change.

Many people in Africa rely on cassava as a primary food source because it grows well in arid soils. But when stressed by drought, the concentration of its chemical defences increase at the same time water to wash out the toxic factors is in short supply. Those dependent on cassava develop an irreversible struggle to walk.

Researchers focused decades of their research in the field and laboratory on grasspea, a tasty legume that also causes tremor, muscle weakness and even paralysis in those who depend upon it for sustenance.

Unfortunately, Palmer said, people may well become increasingly exposed to potentially toxic plants as the climate warms and the global population expands, especially in low-income countries.

This is very concerning, particularly because many people are going to need to rely on these crops in the future, she said.

Spencer believes the exposome - the food we eat, the air we breathe, the chemicals we are unwittingly exposed to - is every bit as important in determining human health and preventing disease.

Prevention of brain disease is our principal goal-seeking and understanding the chemical causes of disease and minimizing human exposure, Spencer said.

(This story has been published from a wire agency feed without modifications to the text. Only the headline has been changed. )

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Heres why not all plant-based diets are good for you - Hindustan Times

RESEARCH TRIANGLE PARK, N.C., Nov. 4, 2019 /PRNewswire/ -- T3D Therapeutics, a clinical stage drug development company engaged in the development of T3D-959, a new orally administered treatment for Alzheimer's disease (AD), announced today that it has closed on a $15 million financing from a cornerstone investor. These funds, along with support from the National Institute on Aging (NIA), part of NIH, completes the funding needed to begin the PIONEER Study of T3D-959, a novel, metabolic-focused AD drug treatment.

"We believe T3D-959 has the potential to be Alzheimer's disease remedial, to either slow, stop, or even reverse the course of disease as a single drug therapy," said Chief Executive OfficerJohn Didsbury, Ph.D. "Our drug works to overcome aberrant glucose (sugar) and lipid (fat) metabolism in the brain that is inherent in AD. This dysfunctional metabolism causes protein mis-folding which in turn leads to plaques, tangles and inflammation."

Warren Strittmatter, M.D., Chief Medical Officer of T3D Therapeutics,Emeritus Professor of Neurology at Duke University Medical Center and Alzheimer's Association Zenith Award winner said, "We are eager to expand our testing of T3D-959 in Alzheimer's patients in this new Phase 2 study since it uniquely targets mechanisms which we believe underlie the development of the memory deficits in this disorder."

About PIONEER

The Phase 2 PIONEER study (Prospective therapy to Inhibit and Overcome Alzheimer's Disease Neurodegeneration via Brain EnErgetics and Metabolism Restoration) is expected to initiate patient dosing in early 2020. PIONEER is adouble-blind, placebo-controlled, parallel-group Phase 2 safety and efficacy study expected to enroll up to 256 adults with mild-to-moderate Alzheimer's disease (MMSE 16-26). PIONEER will enroll subjects who will receive one of three different doses of T3D-959 or a placebo for 24 weeks. PIONEER is projected to start enrolling subjects in the first quarter of 2020.

PIONEER is supported by the NIA under award number R01AG061122.

About T3D Therapeutics, Inc.

T3D Therapeutics, Inc. is a privately-held, Research Triangle Park, NC-based company. The Company has an exclusive license to T3D-959, its lead product candidate, and a platform of structurally-related molecules. T3D Therapeutics' mission is to develop and commercialize T3D-959 for the treatment of Alzheimer's disease and Mild Cognitive Impairment. T3D-959 is a small molecule, orally-delivered, brain-penetrating dual nuclear receptor agonist designed to improve glucose and lipid metabolism dysfunctions present in AD and other neurodegenerative disorders.

For more information visit http://www.t3dtherapeutics.com/.

Investor Contact|

John Didsbury, Ph.D., CEOT3D Therapeutics, Inc.1-919-237-4897Email: info@t3dtherapeutics.com

View original content:http://www.prnewswire.com/news-releases/t3d-therapeutics-closes-15m-financing-to-advance-phase-2-development-of-t3d-959-in-a-new-approach-to-treating-alzheimers-disease-300950374.html

SOURCE T3D Therapeutics, Inc.

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T3D Therapeutics Closes $15M Financing to Advance Phase 2 Development of T3D-959 in a New Approach to Treating Alzheimer's Disease. - BioSpace

Related video above: Researchers Developing Most Powerful MRI Hope to Help Detect Illnesses Like Alzheimers Disease SoonerAuthorities in China have approved a drug for the treatment of Alzheimer's disease, the first new medicine with the potential to treat the cognitive disorder in 17 years.The seaweed-based drug, called Oligomannate, can be used for the treatment of mild to moderate Alzheimer's, according to a statement from China's drug safety agency. The approval is conditional however, meaning that while it can go on sale during additional clinical trials, it will be strictly monitored and could be withdrawn should any safety issues arise.In September, the team behind the new drug, led by Geng Meiyu at the Shanghai Institute of Materia Medica under the Chinese Academy of Sciences, said they were inspired to look into seaweed due to the relatively low incidence of Alzheimer's among people who consume it regularly.In a paper in the journal Cell Research, Geng's team described how a sugar contained within seaweed suppresses certain bacteria contained in the gut which can cause neural degeneration and inflammation of the brain, leading to Alzheimer's.This mechanism was confirmed during a clinical trial carried out by Green Valley, a Shanghai-based pharmaceutical company that will be bringing the new drug to market.Conducted on 818 patients, the trial found that Oligomannate -- which is derived from brown algae -- can statistically improve cognitive function among people with Alzheimer's in as little as four weeks, according to a statement from Green Valley."These results advance our understanding of the mechanisms that play a role in Alzheimer's disease and imply that the gut microbiome is a valid target for the development of therapies," neurologist Philip Scheltens, who advises Green Valley and heads the Alzheimer Center Amsterdam, said in the statement.The company said Oligomannate will be available in China "very soon," and it is currently seeking approval to market it abroad, with plans to launch third-phase clinical trials in the US and Europe in early 2020.Alzheimer's disease, which starts with memory loss and escalates to severe brain damage, is believed to cause 60% to 70% of the cases of dementia reported worldwide, according to the World Health Organization. Dementia affects an estimated 50 million people worldwide, including 9.5 million people in mainland China, Hong Kong and Taiwan.Named after Alois Alzheimer, the neuropathologist who discovered the disease in 1906, it has so far confounded researchers and pharmaceutical companies.In October, US pharmaceutical giant Biogen said it would pursue Food and Drug Administration (FDA) approval for an experimental treatment called aducanumab, after announcing in March it was canceling a large clinical trial for the drug.Johnson & Johnson, Merck, Pfizer and Eli Lilly have all previously abandoned projects to develop a drug for Alzheimer's after unsatisfactory clinical data.

Related video above: Researchers Developing Most Powerful MRI Hope to Help Detect Illnesses Like Alzheimers Disease Sooner

Authorities in China have approved a drug for the treatment of Alzheimer's disease, the first new medicine with the potential to treat the cognitive disorder in 17 years.

The seaweed-based drug, called Oligomannate, can be used for the treatment of mild to moderate Alzheimer's, according to a statement from China's drug safety agency. The approval is conditional however, meaning that while it can go on sale during additional clinical trials, it will be strictly monitored and could be withdrawn should any safety issues arise.

In September, the team behind the new drug, led by Geng Meiyu at the Shanghai Institute of Materia Medica under the Chinese Academy of Sciences, said they were inspired to look into seaweed due to the relatively low incidence of Alzheimer's among people who consume it regularly.

In a paper in the journal Cell Research, Geng's team described how a sugar contained within seaweed suppresses certain bacteria contained in the gut which can cause neural degeneration and inflammation of the brain, leading to Alzheimer's.

This mechanism was confirmed during a clinical trial carried out by Green Valley, a Shanghai-based pharmaceutical company that will be bringing the new drug to market.

Conducted on 818 patients, the trial found that Oligomannate -- which is derived from brown algae -- can statistically improve cognitive function among people with Alzheimer's in as little as four weeks, according to a statement from Green Valley.

"These results advance our understanding of the mechanisms that play a role in Alzheimer's disease and imply that the gut microbiome is a valid target for the development of therapies," neurologist Philip Scheltens, who advises Green Valley and heads the Alzheimer Center Amsterdam, said in the statement.

The company said Oligomannate will be available in China "very soon," and it is currently seeking approval to market it abroad, with plans to launch third-phase clinical trials in the US and Europe in early 2020.

Alzheimer's disease, which starts with memory loss and escalates to severe brain damage, is believed to cause 60% to 70% of the cases of dementia reported worldwide, according to the World Health Organization. Dementia affects an estimated 50 million people worldwide, including 9.5 million people in mainland China, Hong Kong and Taiwan.

Named after Alois Alzheimer, the neuropathologist who discovered the disease in 1906, it has so far confounded researchers and pharmaceutical companies.

In October, US pharmaceutical giant Biogen said it would pursue Food and Drug Administration (FDA) approval for an experimental treatment called aducanumab, after announcing in March it was canceling a large clinical trial for the drug.

Johnson & Johnson, Merck, Pfizer and Eli Lilly have all previously abandoned projects to develop a drug for Alzheimer's after unsatisfactory clinical data.

More:
China approves seaweed-based Alzheimer's drug. It's the first new one in 17 years - WAPT Jackson

New York, Nov. 04, 2019 (GLOBE NEWSWIRE) -- Reportlinker.com announces the release of the report "Europe Pacemakers Market to 2027 - Regional Analysis and Forecasts By Product Type By Technology, By End User, and Country" - https://www.reportlinker.com/p05806319/?utm_source=GNW

The electronic medical implant is an emerging field in the medical industry and has led to various developments of the products, in the field of cardiology, neurology, and otology.Many of the market players are developing novel products in order to minimize the burden of cardiovascular diseases, neurological disorders, and hearing disorders.

For instance, in November 2017, Medtronic launched Azure pacemakers with BlueSync technology that increases the life of the pacemakers, thus reducing the number of device replacements.It also enables to secure and automatic wireless data transmission to physicians.

Similarly, in July 2016, BIOTRONIK headquartered in Germany received CE approval for its new Edora pacemakers and cardiac resynchronization therapy pacemakers (CRT-Ps). Moreover, the presence of pacemaker manufacturers in the European region is also likely to influence the pacemaker market in the European region. Osypka Medical GmbH, Cardiac Impulse S.R.L., Sorin Biomedica C.R.M., S.R.L. are manufacturers located in Europe.In 2018, Europe pacemaker market held a market share of 22.8% of the global pacemaker market. The implantable pacemakers segment expected to dominate its market share and was valued at US$ 855.5 Mn in 2018 and is anticipated to reach US$ 1,687.2 Mn by 2027. On the other hand, implantable pacemakers segment is also anticipated to witness the fastest growth rate of 8.0% during the forecast period, 2019 to 2027.Similarly, in 2018 single-chambered pacemaker segment by technology was valued at US$ 890.2 Mn in 2018 and is anticipated to reach US$ 1,736.8 Mn by 2027 and is also expected to grow at the fastest growth rate of 7.9% during the forecast period.Furthermore, the hospitals & clinics segment held the largest market share of is also anticipated to witness the fastest growth rate of 8.0% during the forecast period, 2019 to 2027. This segment is also expected to dominate the market in 2027 as it is the primary care center for most of the population.Some of the major primary and secondary sources for endodontic devices included in the report are, European Commission, European Society of Cardiology, World Health Organization, European Patent Office, International Trade Administration (ITA) among others.Read the full report: https://www.reportlinker.com/p05806319/?utm_source=GNW

About ReportlinkerReportLinker is an award-winning market research solution. Reportlinker finds and organizes the latest industry data so you get all the market research you need - instantly, in one place.

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The Europe pacemaker market is expected to reach US$ 2,408.5 Mn in 2027 from US$ 1,248.7 Mn in 2018 - GlobeNewswire