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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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Source: Yale

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

About UTSouthwestern Medical Center

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

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

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

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

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

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

Click here for more coverage of CMSC 2024.

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

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

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

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

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

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

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

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

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

Italo Linfante

Following the recent publication in Stroke: Vascular and Interventional Neurology of results from HEMERA-1, a prospective, multicentre trial evaluating the safety of novel neuroprotective agent PP-007 (Prolong Pharmaceuticals) alongside mechanical thrombectomy in acute stroke patients, lead investigator Italo Linfante (Miami Neuroscience Institute, Miami, USA) delves deeper into the data and discusses some of the studys wider implications with NeuroNews.

What is the background to this study, and why did you and your co-investigators initiate it?

Several randomised clinical trials have shown overwhelming superiority of mechanical thrombectomy over medical management for patients with acute stroke secondary to large vessel occlusion (LVO). In these trials and in large-volume case series post trials, despite high rates of complete recanalisation of the occluded vessel, functional independence at 90 days ranges approximately between 4171% of patients.13

In experimental ischaemia models, middle cerebral artery occlusion (MCAO) induces redistribution of cerebral blood flow (CBF), and activation and engagement of leptomeningeal anastomoses (LMA). The amount of redistribution and increase of CBF in LMA can significantly influence final infarct volume.68 In fact, in experimental ischaemia models and in patients with acute stroke secondary to LVO, increased CBF in LMA reduces the activation of several neurotoxic molecules in penumbral tissue, slows core expansion, and ultimately induces protection from neuronal ischaemic injury. Conversely, poor blood flow in LMA is associated with a faster growth of the ischaemic core.6

PEGylated bovine carboxyhaemoglobin, or PP-007, is a carbon monoxide (CO)-releasing and oxygen-transfer molecule with pleotropic neuroprotective effects. As demonstrated in several experimental ischaemia models, such as temporary rats MCAOs, the neuroprotection induced by PP-007 is due to a combination of: increased blood flow in pial collaterals; optimisation of oxygen transport in ischaemic tissue; and plasma expansion effect secondary to the pegylated nature of the compound.1216 Furthermore, since PP-007 also acts as a CO donor and small amounts of CO were found to have anti-inflammatory properties, PP-007 was observed to reduce proinflammatory cytokines.8,13 Dose escalation studies were performed in normal volunteers, patients with sickle cell anaemia and patients with subarachnoid haemorrhage too.

Could you very briefly describe the design and methodology of the study?

We aimed to evaluate the safety and feasibility of PP-007 in acute stroke patients undergoing mechanical thrombectomy. HEMERA-1 was a Phase 1, multicentre, prospective randomised controlled clinical trial. Anterior-circulation LVO patients were assigned in a 3:1 ratio to receive either PP-007 (320mg/kg; 30-minute bolus followed by two-hour infusion) plus mechanical thrombectomy or mechanical thrombectomy alone within 24 hours after symptom onset. Comprehensive safety evaluation was performed by an independent data safety monitoring board (DSMB) and an independent imaging core lab.

Could you briefly summarise the key findings of HEMERA-1, now published in Stroke: Vascular and Interventional Neurology?

From 10 January 2021 to 30 June 2022, a total of 17 patients were recruited. Age, baseline National Institutes of Health stroke scale (NIHSS) and Alberta stroke programme early computed tomography score (ASPECTS) were 74.812.7 years, 17.34.2, and 7.91.8, respectively. Twelve patients were randomised PP-007 plus mechanical thrombectomyone was randomised but not treatedand four patients were randomised to mechanical thrombectomy alone. Recanalisation of the occluded vessel was achieved in all patients.

Was there anything in these results, positive or negative, that surprised you?

No significant safety concerns were identified for the adjunctive use of PP-007 in patients undergoing mechanical thrombectomy after the DSMB reviewed all patients data in detail for every organ system, independently from the investigators. A transient systolic blood pressure increase (2040mmHg) during the bolus was observed in all PP-007 patients without any clinical consequences.

Do you have any concerns at all regarding the transient increase in systolic blood pressure seen in patients treated with PP-007 in the trial?

No, because the increase in blood pressure is consistent with the plasma-expander properties of PP-007. This temporary increase in blood pressure had no safety concerns, as adjudicated by the DSMB and the imaging core lab.

It is noted in the paper that patients treated with intravenous thrombolysis were not eligible for HEMERA-1do you think it is inherently likely that subsequent studies can produce even more positive outcomes, given the known benefits of thrombolytics may be compounded by the neuroprotective effects of PP-007?

As per US Food and Drug Administration (FDA) request, to avoid drug-drug interaction, we did not enrol patients who received alteplase (tPA) or tenecteplase (TNK) in HEMERA-1. Once the data were analysed and adjudicated to be safe, we then enrolled an additional 14 patients to evaluate safety of the combination of tPA or TNK, and PP-007. The data were reviewed by two additional DSMB meetings and a core imaging lab independent from the investigators. No safety concerns were found, with the data set to be submitted for publication.

With this study having been successful, can you shed any light on the randomised controlled trial that will now follow to assess PP-007s efficacy?

We are currently planning a multicentre, Phase 2b/3 randomised clinical trial for efficacy. Patients with acute stroke secondary to LVO undergoing mechanical thrombectomy will be randomly assigned to receive PP-007 or placebo. The trial will have an adaptive design and a shift analysis of the modified Rankin scale (mRS) at 90 days as its primary endpoint. Secondary endpoints will include NIHSS changes, infarct growth on follow-up imaging etc. We hope to submit the randomised trial design to the US FDA by the end of the year.

How many stroke patients could be positively impacted by this neuroprotective drug if it does continue to progress through trials and into clinical practiceand how much of a difference could it make for them?

Data from the American Heart Association (AHA) report that, every year, more than 750,000 people in the USA have a stroke, and 87% of them are ischaemic.15 In my humble opinion, if the trial will show efficacy, all ischaemic stroke patients can be potentially treated with PP-007. In addition, if PP-007 is beneficial for ischaemic stroke patients, perhaps this advanced molecule could be used in other organs affected by ischaemic conditions.

There have been some fairly mixed data and findings on neuroprotection over the past few yearswhat do you think the overall landscape looks like for neuroprotection, and are we getting closer to elucidating its potential role in acute stroke care?

Many promising therapeutic agents for neuroprotection have been identified to target the complex pathophysiological events occurring at the level of the neurovascular unit during ischaemia.45 However, none of these agents have proven to be beneficial in clinical studies to date. It must be considered that most of these studies predated the mechanical thrombectomy era and, most likely, neuroprotection may not be evident without effective recanalisation of the occluded artery. In my opinionnow that we are in the mechanical thrombectomy era, with high recanalisation ratesthere will be a tremendous effort to develop pharmacological agents that are able to slow down core expansion and preserve the ischaemic penumbra to improve outcomes in patients with acute stroke secondary to large-artery occlusions.

References:

Original post:
Positive HEMERA-1 data pave the way for further neuroprotection trials during 'thrombectomy era' - NeuroNews International

Summary: A new study finds that reports of cognitive decline from patients and their partners are linked to the accumulation of tau tangles, a hallmark of Alzheimers disease. This underscores the importance of addressing memory concerns early.

The study, involving 675 participants, used PET imaging to detect tau and amyloid beta, finding a correlation between these markers and self-reported cognitive decline.

Key Facts:

Source: Brigham and Womens Hospital

A new study adds further evidence that when a patient or family member notices signs of persistent memory loss, its important to speak with a doctor.

While there are many reasons why someones memory may change, researchers fromMass General Brighamwho are studying patients prior to diagnosis with Alzheimers disease found changes in the brain when patients and their study partnersthose who could answer questions about their daily cognitive functionreported a decline in cognition.

Using imaging, the researchers found reports of cognitive decline were associated with accumulation of tau tanglesa hallmark of Alzheimers disease.

Results are published inNeurology,the medical journal of the American Academy of Neurology.

Something as simple as asking about memory complaints can track with disease severity at the preclinical stage of Alzheimers disease, said senior author Rebecca E. Amariglio, PhD, of the Department of Neurology at Brigham and Womens Hospital. Amariglio is a clinical neuropsychologist at both Brigham and Womens Hospital and Massachusetts General Hospital, the founding members of Mass General Brigham.

We now understand that changes in the brain due to Alzheimers disease start well before patients show clinical symptoms detected by a doctor. There is increasing evidence that individuals themselves or a close family member may notice changes in memory, even before a clinical measure picks up evidence of cognitive impairment.

The new study, led by first author Michalina F. Jadick, included researchers from across the Brigham and Mass General. The research team designed their study to include participants from the Anti-Amyloid Treatment in Asymptomatic AD/Longitudinal Evaluation of Amyloid Risk (A4/LEARN) and Neurodegeneration studies and the Harvard Aging Brain Study and affiliated studies.

Participants were cognitively unimpaired individuals at risk but not yet diagnosed with Alzheimers disease. Each participant and respective study partner completed evaluations of cognitive function for the participant. Each participant also underwent PET imaging to detect levels of tau and amyloid beta.

Across 675 participants, the team found that both amyloid and tau were associated with greater self-reported decline in cognitive function. The team also found that subjective reports from patients and their partners complemented objective tests of cognitive performance.

The authors note that the study was limited by the fact that most participants were white and highly educated. Future studies that include more diverse participants and follow participants in the longer term are needed.

Amariglio cautions that noticing a change in cognition does not mean that one should leap to the conclusion that a person has Alzheimers disease. However, a patients or family members concerns should not be dismissed if they are worried about cognition.

Authorship:In addition to Jadick and Amariglio, Mass General Brigham authors include Hannah Klinger (MGH), Rachel F. Buckley (MGH, BWH), Gad A. Marshall (MGH, BWH), Patrizia Vannini (MGH, BWH), Dorene M. Rentz (MGH, BWH), Keith A. Johnson (MGH, BWH), Reisa A. Sperling (MGH, BWH), Talia Robinson (BWH), and Michelle E. Farrell (BWH).

Disclosures:Marshall has received research salary support for serving as a site principal investigator for clinical trials funded by Eisai Inc., Eli Lilly and Company, and Genentech which are not related to the content in the manuscript. Johnson is a consultant for Merck and Novartis.

Sperling has served as a paid consultant for AbbVie, ACImmune, Acumen, Alector, Bristol Myers Squibb, Genentech, Ionis, Janssen, Nervgen, Oligomerix, Prothena, Roche, and Vaxxinity, receives research funding from Eisai and Eli Lilly for public-private partnership clinical trials, receives grant funding from the National Institute on Aging/NIH (P01AG036694), GHR Foundation, and the Alzheimers Association. Johnson (spouse) reports consulting fees from Merck and Novartis.

Author: Cassandra Falone Source: Brigham and Womens Hospital Contact: Cassandra Falone Brigham and Womens Hospital Image: The image is credited to Neuroscience News

Original Research: Closed access. Associations Between Self and Study Partner Report of Cognitive Decline With Regional Tau in a Multicohort Study by Rebecca E. Amariglio et al. Neurology

Abstract

Associations Between Self and Study Partner Report of Cognitive Decline With Regional Tau in a Multicohort Study

Self-reported cognitive decline is an early behavioral manifestation of Alzheimer disease (AD) at the preclinical stage, often believed to precede concerns reported by a study partner. Previous work shows cross-sectional associations with -amyloid (A) status and self-reported and study partner-reported cognitive decline, but less is known about their associations with tau deposition, particularly among those with preclinical AD.

This cross-sectional study included participants from the Anti-Amyloid Treatment in Asymptomatic AD/Longitudinal Evaluation of Amyloid Risk and Neurodegeneration studies (N = 444) and the Harvard Aging Brain Study and affiliated studies (N = 231), which resulted in a cognitively unimpaired (CU) sample of individuals with both nonelevated (A) and elevated A (A+). All participants and study partners completed the Cognitive Function Index (CFI).

Two regional tau composites were derived by averaging flortaucipir PET uptake in the medial temporal lobe (MTL) and neocortex (NEO). Global A PET was measured in Centiloids (CLs) with A+ >26 CL. We conducted multiple linear regression analyses to test associations between tau PET and CFI, covarying for amyloid, age, sex, education, and cohort. We also controlled for objective cognitive performance, measured using the Preclinical Alzheimer Cognitive Composite (PACC).

Across 675 CU participants (age = 72.3 6.6 years, female = 59%, A+ = 60%), greater tau was associated with greater self-CFI (MTL: = 0.28 [0.12, 0.44],p< 0.001, and NEO: = 0.26 [0.09, 0.42],p= 0.002) and study partner CFI (MTL: = 0.28 [0.14, 0.41],p< 0.001, and NEO: = 0.31 [0.17, 0.44],p< 0.001). Significant associations between both CFI measures and MTL/NEO tau PET were driven by A+. Continuous A showed an independent effect on CFI in addition to MTL and NEO tau for both self-CFI and study partner CFI. Self-CFI ( = 0.01 [0.001, 0.02],p= 0.03), study partner CFI ( = 0.01 [0.003, 0.02],p= 0.01), and the PACC ( = 0.02 [0.03, 0.01],p< 0.001) were independently associated with MTL tau, but for NEO tau, PACC ( = 0.02 [0.03, 0.01],p< 0.001) and study partner report ( = 0.01 [0.004, 0.02],p= 0.002) were associated, but not self-CFI ( = 0.01 [0.001, 0.02],p= 0.10).

Both self-report and study partner report showed associations with tau in addition to A. Additionally, self-report and study partner report were associated with tau above and beyond performance on a neuropsychological composite.

Stratification analyses by A status indicate that associations between self-reported and study partner-reported cognitive concerns with regional tau are driven by those at the preclinical stage of AD, suggesting that both are useful to collect on the early AD continuum.

Read this article:
Early Memory Complaints Linked to Alzheimers Brain Changes - Neuroscience News

WATCH TIME: 4 minutes

Welcome to this special edition of Neurology News Network. Im Marco Meglio. This weeks episode is centered around the 2024 CMSC Annual Meeting.

New findings from the phase 4 CHIMES (NCT04377555) trial showed effective control of multiple sclerosis (MS) disease activity among Black/African American and Hispanic/Latino patients with relapsing MS after 1 year of ocrelizumab (Ocrevus; Genentech) treatment. The data was consistent with safety findings from prior studies and suggest that ocrelizumab is a suitable treatment for this diverse patient population. In the analysis, approximately half of Black/African American patients with RMS (46.0%) and more than half of Hispanic/Latino patients with RMS (58.0%) achieved 48-week no evidence of disease activity (NEDA) following treatment with ocrelizumab. A majority of the Black/African American and Hispanic/Latino patients with RMS reported no relapses (94.7%; 95.7%, respectively), 24-week confirmed disability progression (94.7%; 94.2%, respectively), or T1 gadolinium-enhancing lesions (94.7%; 97.1%, respectively).

Findings from a single-center, real-world cohort of older patients with relapsing multiple sclerosis (MS) showed that cladribine (Mavenclad; EMD Serono) was safe and well tolerated for a 2-year period after switching from a previous disease-modifying therapy (DMT). These data appear encouraging, as an aging population often faces increased comorbid conditions. Cladribine was well tolerated, with lymphopenia, upper respiratory tract infection, urinary tract infection, fatigue, and headache occurring in less than 5% of both the full cohort (n = 75) and a subgroup of those older than 50 (n = 40).

New findings from a small sample survey presented at the 2024 CMSC Annual Meeting, held May 29 to June 2, revealed high rates of burnout and job stress among physicians treating patients with MS in the United States (US), while providing key insights into the sources of stress and burnout in the field.1 The hope is that these insights can help facilitate systemic changes to support MS physicians to offer the quality care for their patients. Among 115 (85%) of the total respondents (n = 136) who completed the survey, 50% responded that they were burned out or beginning to experience burnout, and 52% of respondents reported great job stress. According to the Mini Z scoring system, 74% of respondents cited electronic medical records (EMRs) as a source of frustration. In the survey, 61% reported a high degree of EMR-related stress, 60% responded that time for documentation was marginal or poor, and 59% noted that time spent at home on EMR was moderately high or excessive.

For more direct access to expert insight, head to NeurologyLive.com. This has been Neurology News Network. Thanks for watching.

Continue reading here:
Ocrelizumab Effective in Diverse Populations, Cladribine Safe After Switching DMTs, High Rates of Burnout for MS ... - Neurology Live

Scientists have designed and implanted a transparent window in a patients skull and then used functional ultrasound imaging (fUSI) through it to collect high-resolution brain imaging data.

The results of the study are published in the journal Science Translational Medicine.

This is the first time anyone had applied functional ultrasound imaging through a skull replacement in an awake, behaving human performing a task, saysco-author Charles Liu, a professor of clinical neurological surgery, at the Keck School of Medicine, the University of Southern California.

The ability to extract this type of information noninvasively through a window is pretty significant, particularly since many of the patients who require skull repair have or will develop neurological disabilities.

In addition, windows can be surgically implanted in patients with intact skulls if functional information can help with diagnosis and treatment.

The research participant, 39-year-oldJared Hager, sustained a traumatic brain injury (TBI)from a skateboarding accident in 2019.Half of Hagers skull was removed during emergency surgery to relieve pressure on his brain, which left part of his brain covered only by skin and connective tissue.

Functional ultrasound imaging records brain activity by measuring changes in blood flow. However, it cannot be done through the skull or a traditional implant.

So, after testing in animal models, Liu and colleagues designed a Hager custom skull implant made from clear polymethyl methacrylate (PMMA).

They then collected fUSI data while Hager completed several tasks, before his surgery and after the clear implant was installed, to compare them.

The fidelity of course decreased, but importantly, our research showed that its still high enough to be useful, Liu said.

And unlike other brain-computer interface platforms, which require electrodes to be implanted in the brain, this has far less barriers to adoption.

Original post:
New brain imaging technique through clear window in skull - Cosmos

Researchers from Mass General Brigham have found that self-reports of cognitive decline by patients and their partners are linked to the accumulation of tau in the brain, a marker of Alzheimers disease. Credit: SciTechDaily.com

A study reveals that reports of memory decline by patients and partners were associated with the accumulation of tau, a hallmark of Alzheimers disease.

New research adds further evidence that when a patient or family member notices signs of persistent memory loss, its important to speak with a doctor. While there are many reasons why someones memory may change, researchers from Mass General Brigham who are studying patients prior to diagnosis with Alzheimers disease found changes in the brain when patients and their study partnersthose who could answer questions about their daily cognitive functionreported a decline in cognition.

Using imaging, the researchers found reports of cognitive decline were associated with accumulation of tau tanglesa hallmark of Alzheimers disease. Results are published today (May 29) in the journal Neurology, the medical journal of the American Academy of Neurology.

Something as simple as asking about memory complaints can track with disease severity at the preclinical stage of Alzheimers disease, said senior author Rebecca E. Amariglio, PhD, of the Department of Neurology at Brigham and Womens Hospital. Amariglio is a clinical neuropsychologist at both Brigham and Womens Hospital and Massachusetts General Hospital, the founding members of Mass General Brigham.

We now understand that changes in the brain due to Alzheimers disease start well before patients show clinical symptoms detected by a doctor. There is increasing evidence that individuals themselves or a close family member may notice changes in memory, even before a clinical measure picks up evidence of cognitive impairment.

The new study, led by first author Michalina F. Jadick, included researchers from across the Brigham and Mass General. The research team designed their study to include participants from the Anti-Amyloid Treatment in Asymptomatic AD/Longitudinal Evaluation of Amyloid Risk (A4/LEARN) and Neurodegeneration studies and the Harvard Aging Brain Study and affiliated studies. Participants were cognitively unimpaired individuals at risk but not yet diagnosed with Alzheimers disease. Each participant and respective study partner completed evaluations of cognitive function for the participant. Each participant also underwent PET imaging to detect levels of tau and amyloid beta.

Across 675 participants, the team found that both amyloid and tau were associated with greater self-reported decline in cognitive function. The team also found that subjective reports from patients and their partners complemented objective tests of cognitive performance.

The authors note that the study was limited by the fact that most participants were white and highly educated. Future studies that include more diverse participants and follow participants in the longer term are needed.

Amariglio cautions that noticing a change in cognition does not mean that one should leap to the conclusion that a person has Alzheimers disease. However, a patients or family members concerns should not be dismissed if they are worried about cognition.

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

Authorship: In addition to Jadick and Amariglio, Mass General Brigham authors include Hannah Klinger (MGH), Rachel F. Buckley (MGH, BWH), Gad A. Marshall (MGH, BWH), Patrizia Vannini (MGH, BWH), Dorene M. Rentz (MGH, BWH), Keith A. Johnson (MGH, BWH), Reisa A. Sperling (MGH, BWH), Talia Robinson (BWH), and Michelle E. Farrell (BWH).

Disclosures: Marshall has received research salary support for serving as a site principal investigator for clinical trials funded by Eisai Inc., Eli Lilly and Company, and Genentech which are not related to the content in the manuscript. Johnson is a consultant for Merck and Novartis. Sperling has served as a paid consultant for AbbVie, ACImmune, Acumen, Alector, Bristol Myers Squibb, Genentech, Ionis, Janssen, Nervgen, Oligomerix, Prothena, Roche, and Vaxxinity, receives research funding from Eisai and Eli Lilly for public-private partnership clinical trials, receives grant funding from the National Institute on Aging/NIH (P01AG036694), GHR Foundation, and the Alzheimers Association. Johnson (spouse) reports consulting fees from Merck and Novartis.

Read more here:
Unlocking Alzheimer's: Memory Complaints Can Predict Biological Changes in the Brain - SciTechDaily

Neurological disorders including addiction, depression, and obsessive-compulsive disorder (OCD) are often characterised by complex pathologies involving multiple brain regions and circuits.

These conditions are difficult to treat due to the intricate and poorly understood nature of brain functions and the challenge of delivering therapies to deep brain structures without invasive procedures.

Now, an interdisciplinary team of researchers led by Friedhelm Hummel and postdoc Pierre Vassiliadis are pioneering transcranial Temporal Interference Electric Stimulation (tTIS). The method targets deep brain regions that are the control centres of several important cognitive functions and involved in different neurological and psychiatric pathologies. The research is detailed in Nature Human Behaviour.

Invasive deep brain stimulation [DBS] has already successfully been applied to the deeply seated neural control centres in order to curb addiction and treat Parkinson, OCD or depression, Hummel said in a statement. The key difference with our approach is that it is non-invasive, meaning that we use low-level electrical stimulation on the scalp to target these regions.

Lead author Vassiliadis, a medical doctor with a joint PhD, describes tTIS as using two pairs of electrodes attached to the scalp to apply weak electrical fields inside the brain.

"Up until now, we couldnt specifically target these regions with non-invasive techniques, as the low-level electrical fields would stimulate all the regions between the skull and the deeper zones, rendering any treatments ineffective. This approach allows us to selectively stimulate deep brain regions that are important in neuropsychiatric disorders," he said.

The technique is based on the concept of temporal interference, initially explored in rodent models, and now translated to human applications by the EPFL team.

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In this experiment, one pair of electrodes is set to a frequency of 2,000Hz, while another is set to 2,080Hz. Thanks to detailed computational models of the brain structure, the electrodes are specifically positioned on the scalp to ensure that their signals intersect in the target region.

The frequency disparity of 80Hz between the two currents becomes the effective stimulation frequency within the target zone. The high base frequencies do not stimulate neural activity directly, leaving the intervening brain tissue unaffected and focusing the effect solely on the targeted region.

According to EPFL, the focus of this latest research is the human striatum, which is involved in decision making functions, such as reward.

"We're examining how reinforcement learning, essentially how we learn through rewards, can be influenced by targeting specific brain frequencies," said Vassiliadis. By applying stimulation of the striatum at 80Hz, the team found they could disrupt its normal functioning, directly affecting the learning process.

The therapeutic potential of their work could have a positive impact on conditions like addiction, apathy and depression, where reward mechanisms play a crucial role.

"In addiction, for example, people tend to over-approach rewards. Our method could help reduce this pathological overemphasis," said Vassiliadis.

Furthermore, the team is exploring how different stimulation patterns can not only disrupt but also potentially enhance brain functions. "This first step was to prove the hypothesis of 80Hz affecting the striatum, and we did it by disrupting its functioning. Our research also shows promise in improving motor behaviour and increasing striatum activity, particularly in older adults with reduced learning abilities," said Vassiliadis.

Visit our jobs sitehttps://jobs.theengineer.co.uk/to find out about some of the latest career opportunities at industry's biggest employers

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Non-invasive brain stimulation shows promise for neurological therapy - The Engineer

THURSDAY, May 30, 2024 (HealthDay News) -- Individuals who self-report and whose partners report cognitive decline have greater tau, which is driven by elevated beta-amyloid (A), according to a study published online May 29 in Neurology.

Michalina F. Jadick, from Massachusetts General Hospital in Boston, and colleagues conducted a cross-sectional study to examine associations of self-reported and study partner-reported cognitive decline with tau deposition, especially among those with preclinical Alzheimer disease. Flortaucipir positron emission tomography (PET) uptake was averaged in the medial temporal lobe (MTL) and neocortex (NEO) to derive two regional tau composites. Associations between tau PET and the Cognitive Function Index (CFI) were examined among 675 cognitively unimpaired individuals.

The researchers found that greater tau was associated with greater self-reported CFI ( = 0.28 and 0.26 for MTL and NEO, respectively) and study partner-reported CFI ( = 0.28 and 0.31 for MTL and NEO, respectively). Elevated A was the driver of the significant associations between both CFI measures and MTL/NEO tau PET. For both self- and study partner-reported CFI, continuous A showed an independent effect on CFI in addition to MTL and NEO tau. Independent associations were seen for self-reported CFI, study partner-reported CFI, and the Preclinical Alzheimer Cognitive Composite (PACC) with MTL tau; independent associations were seen for study partner-reported CFI and PACC, but not self-reported CFI, with NEO tau.

"Our study found early suspicions of memory problems by both participants and the people who knew them well were linked to higher levels of tau tangles in the brain," coauthor Rebecca E. Amariglio, Ph.D., from Harvard Medical School in Boston, said in a statement.

Several authors disclosed ties to the biopharmaceutical industry.

Abstract/Full Text (subscription or payment may be required)

Continue reading here:
Self-, Partner-Reported Cognitive Decline Linked to Tau - HealthDay

Hoff, P. Eugen Bleulers concept of schizophrenia and its relevance to present-day psychiatry. Neuropsychobiology 66, 613 (2012).

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Read the rest here:
Support for network theories of schizophrenia - Nature.com

Japan headquartered pharma company Eisai Co. has announced that its French sales subsidiary Eisai S.A.S. has entered into an agreement to transfer the rights in France, the French Overseas Territories and Algeria (the Territory for the antipsychotic, Loxapac (generic name: loxapine) and the Parkinson's disease treatment ParkinaneLP (generic name: trihexyphenidyl hydrochloride) to CNX Therapeutics, based in UK.

Following the signature of this agreement, a transition period had opened during which the required implementation steps will be carried out in order for CNX to become able to operate directly the business, including the regulatory steps for the transfer of the relevant marketing authorisations andexploitantstatus.

Under the terms of the agreement, Eisai S.A.S. will receive 56.5 million euro as a lump-sum contract payment upon completing the transaction. Eisai anticipates no changes to its consolidated financial forecast for the period ending March 31, 2024.

Eisai S.A.S. acquired the rights to both treatments in the Territory in July 2002 and has been marketing them since. With the conclusion of this agreement, Eisai believes that the value of both treatments in the Territory will be maximised based on CNXs ongoing commitment serving patients in to the fields of psychiatry and neurology.

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French sales subsidiary of Japanese pharma firm Eisai divests rights of neurology drugs for 56.5 M - BSA bureau

Hackensack Meridian Neuroscience Institute at JFK University Medical Center announced today that it has been awarded a major research grant from the National Institute of Neurological Disorders and Stroke, part of the U.S. National Institutes of Health, to study a novel approach on whether the blocking of formation of Neutrophil extracellular traps (NET) provides better outcomes after a Traumatic Brain Injury (TBI). The five-year award of $2,213,750 is part of the highly competitive NIH extramural grant application process that recognizes innovative scientific projects. NIH-funded research has led to scientific breakthroughs and new treatments that help people live longer, healthier lives.

The NIH grant will fund a project entitled Neutrophil Extracellular Traps And Associated Pathogenesis In TBI: A Novel Peptide Therapeutic Strategy proposed by Mohammed Abdul Muneer, MSc, PhD, Research Scientist & Principal Investigator, Hackensack Meridian Neuroscience Institute at JFK University Medical Center, and Associate Professor of Neurology at the Hackensack Meridian School of Medicine.

The work hypothesizes that inhibition of peptidyl arginine deiminase type 4 (PAD4), an enzyme required for NET formation, using PAD4 antagonistic peptide (PAP), will attenuate the formation of NET, NET-induced thrombosis, and will promote neovascularization and functional recovery after TBI.

We are honored to receive this prestigious NIH grant, said Gregory J. Przybylski, M.D., MBA, chairman, Hackensack Meridian Neuroscience Institute at JFK University Medical Center, and Professor of Neurosurgery at the Hackensack Meridian School of Medicine. I congratulate Dr. Muneer and his team for this incredible achievement. This is yet another research grant that he has received from the NIH. It is a testament to his hard work, dedication, and leadership in the neuroscience field.

The Muneer lab at the Hackensack Meridian Neuroscience Institute at JFK University Medical Center seeks to demonstrate a unique therapeutic strategy for TBI focusing on the activation of leukocytes, especially neutrophils that cause the release of nuclear and granular contents to form an extensive web-like structure of DNA called neutrophil extracellular traps (NET). In TBI, the mechanism of injury-induced formation of NET and its mechanistic regulatory role in thrombosis have remained elusive. Moreover, it is unclear whether blocking NET formation provides better outcomes after TBI. Therefore, Dr. Muneers novel research efforts to suppress the formation of NET will provide critical information potentially supporting a valuable new therapeutic strategy to enhance functional recovery following TBI.

My research team and I will study an approach to suppressing the formation of NET, which may be a valuable therapeutic strategy, and analyze the efficacy of the therapy in the functional recovery level after TBI, said Dr. Muneer.

The Neuroscience Institute at JFK University Medical Center has been in existence for over 30 years, said Gay Holstein, PhD, translation research, Neuroscience Institute at JFK University Medical Center. We are honored to receive this research grant and look forward to the findings.

TBI is such an omnipresent problem, its critical to have our talented researchers findings new ways to improve and lengthen lives for this significant patient population, said Ihor Sawczuk, M.D., FACS, president of Academics, Research, and Innovation at Hackensack MeridianHealth, founding chair of the Hackensack MeridianHealthResearch Institute, and associate dean of Clinical Integration and professor and chair emeritus of Urology at the Hackensack Meridian School of Medicine.

Link:
Hackensack Meridian Neuroscience Institute at JFK University Medical Center Receives $2.2 Million Research Grant to ... - Newswise

This is a video synopsis/summary of a panel discussion involving James Howard, MD; Nicholas Silvestri, MD, FAAN; Tuan Vu, MD; Ali Habib, MD; and Beth Stein, MD.

The discussion delves into the administration of treatments for myasthenia gravis (MG), emphasizing its impact on patients' quality of life. Traditionally, Intravenous immunoglobulin (IVIG) has been the go-to therapy for disease exacerbations, but this paradigm is shifting with the emergence of newer therapies, each with its own unique administration methods.

The insidious progression of MG often sets a new normal for patients, leading them to attribute symptoms to aging rather than disease progression. Physicians must engage patients in conversations about the risks and benefits of trying new treatments, challenging the notion that certain limitations are solely due to age.

Moreover, as MG symptoms are brought under control, it's crucial not to attribute every symptom to the disease itself. Patients may have other comorbidities contributing to their symptoms, requiring a comprehensive approach to management.

The term "refractory" is controversial, with physicians acknowledging that almost every patient responds to some degree of treatment. However, there's a push to redefine success in MG management, aiming for optimal control with minimal side effects.

Physicians note varying experiences with treatment efficacy, influenced by factors like patient demographics and practice settings. With the goal of achieving no symptoms and minimal adverse events, the consensus is that a significant portion of patients can achieve better outcomes with current therapies. Practice settings may influence success rates, with university-based practices potentially encountering more complex cases.

Overall, the conversation highlights the need for a patient-centered approach to MG management, with an emphasis on individualized treatment plans and realistic expectations for outcomes.

Video synopsis is AI-generated and reviewed by NeurologyLive editorial staff.

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Quality of Life in MG - Neurology Live

PARAMUS, N.J. , April 9, 2024 /PRNewswire/ -- SK Life Science, Inc. , a U.S. pharmaceutical company in pursuit of developing treatments that will change the future of central nervous system (CNS) disorders, today announced the schedule for two oral and six poster presentations at the American Academy of Neurology (AAN) Annual Meeting taking place April 1318, 2024, virtually and in-person in Denver, Colorado . The data includes a study examining the relative bioavailability of cenobamate as an intact or crushed tablet administered either orally or via nasogastric tube, and a retrospective claims-based analysis comparing the effectiveness of cenobamate in reducing hospitalizations among patients with focal-onset seizures.

"We are looking forward to sharing data on the use and administration of XCOPRI in adults with partial-onset (focal) seizures at this year's AAN meeting," said Louis Ferrari , RPh, MBA, vice president, Medical Affairs. "At SK Life Science we are continually conducting research that will help healthcare professionals and equip them with the information they need to care for patients living with the challenges of epilepsy. We continue to do this via ongoing research, relevant post-hoc analyses, and the publication of real-world data on the use of cenobamate in the U.S. and globally."

Abstracts are available online on the AAN meeting website here and on site at booth #1262. The schedule of oral and poster presentations is detailed below.

Oral Presentations

Title: Comparative Effectiveness of Cenobamate in Reducing Hospitalizations in Patients with Focal-Onset Seizures: A Retrospective Claims-Based Analysis (Urban et al) Session: S29: Epilepsy Diagnostics and Therapeutics Date: Wednesday, April 17 Time: 1:24 PM

Title: Relative Bioavailability of Cenobamate 200 mg Administered as a Crushed Tablet, Either Orally or via Nasogastric Tube, vs an Intact 200-mg Cenobamate Tablet (Vashi et al) Session: S29: Epilepsy Diagnostics and Therapeutics Date: Wednesday, April 17 Time: 1:36 PM

Poster Presentations

Title: Effectiveness Of Cenobamate in Pediatric Patients with Lennox-Gastaut Syndrome: A Retrospective Claims-based Analysis (Keough et al) Session: P1: Epilepsy/Clinical Neurophysiology (EEG): Pediatric Epilepsy 1 Date: Sunday, April 14 Time: 8:00 9:00 AM

Title: Effectiveness Of Cenobamate in Pediatric Patients with Intractable Focal Seizures: A Retrospective Claims-based Analysis (Labiner et al) Session: P2: Epilepsy/Clinical Neurophysiology (EEG): Pediatric Epilepsy 2 Date: Sunday, April 14 Time: 11:45 AM 12:45 PM

Title: Increased Incidence of Comorbidities in Patients with Uncontrolled Epilepsy (Faught et al) Session: P4: Epilepsy/Clinical Neurophysiology (EEG): Epilepsy Co-morbidities and Special Populations Date: Monday, April 15 Time: 11:45 AM 12:45 PM

Title: Effectiveness Of Cenobamate in Postsurgical Patients: A Retrospective Claims-based Analysis (Pellinen et al) Session: P8: Epilepsy/Clinical Neurophysiology (EEG): Anti-seizure Medications: Clinical Trials and Outcomes Date: Tuesday: April 16 Time: 5:30 6:30 PM

Title: Cenobamate Use as Monotherapy: A Retrospective Claims-based Analysis (Becker et al) Session: P8: Epilepsy/Clinical Neurophysiology (EEG): Anti-seizure Medications: Clinical Trials and Outcomes Date: Tuesday, April 16 Time: 5:30 6:30 PM

Title: Dose Reduction Timing for Concomitant Antiseizure Medications: Post-hoc Analysis of a Phase 3, Open-label Study Of Cenobamate For Treatment Of Uncontrolled Focal Seizures (Ferrari et al) Session: P8: Epilepsy/Clinical Neurophysiology (EEG): Anti-seizure Medications: Clinical Trials and Outcomes Date: Tuesday, April 16 Time: 5:30 6:30 PM

AboutXCOPRI (cenobamatetablets) CV Cenobamateis an antiseizure medication (ASM) discovered and developed by SK Biopharmaceuticals and SK Life Science. While theprecise mechanism by whichcenobamateexerts its therapeutic effect is unknown, it is believed toreduce repetitive neuronal firing by inhibiting voltage-gated sodium currents. It is also a positive allosteric modulator of the -aminobutyric acid (GABA A ) ion channel.

Cenobamateis approved in the United States for the treatment ofpartial-onset seizures inadults andis available under the brand name XCOPRI (cenobamatetablets) CV.Cenobamatecan be combined with other ASMs or used alone.The recommended initial dosage ofcenobamateis 12.5 mg once-daily, with titration every two weeks; it is available in six tablet strengths for once-daily dosing: 12.5 mg, 25 mg, 50 mg, 100 mg, 150 mg and 200 mg.

Cenobamateis also approved in the European Union and the United Kingdomfor the adjunctive treatment of focal-onset (partial-onset) seizures with or without secondary generalization in adult patients with seizuresthathave not been adequately controlled despite a history of treatment with at least two anti-epileptic medicinalproductsand is marketed by Angelini Pharma under the brand nameONTOZRY .

Additionally,cenobamateis in clinical development in Asia . Ono Pharmaceutical and Ignis Therapeutics have the rights to develop and commercializecenobamatein Japan and in the Greater China region, respectively.SK Biopharmaceuticals has recently entered into an exclusive licensing agreement with Endo for cenobamate in Canada .

IMPORTANT SAFETY INFORMATION AND INDICATION FOR XCOPRI (cenobamate tablets) CV

DO NOT TAKE XCOPRI IF YOU:

XCOPRI CAN CAUSE SERIOUS SIDE EFFECTS, INCLUDING:

Allergic reactions: XCOPRI can cause serious skin rash or other serious allergic reactions which may affect organs and other parts of your body like the liver or blood cells. You may or may not have a rash with these types of reactions. Call your healthcare provider right away and go to the nearest emergency room if you have any of the following: swelling of your face, eyes, lips, or tongue, trouble swallowing or breathing, a skin rash, hives, fever, swollen glands, or sore throat that does not go away or comes and goes, painful sores in the mouth or around your eyes, yellowing of your skin or eyes, unusual bruising or bleeding, severe fatigue or weakness, severe muscle pain, frequent infections, or infections that do not go away. Take XCOPRI exactly as your healthcare provider tells you to take it. It is very important to increase your dose of XCOPRI slowly, as instructed by your healthcare provider.

QT shortening: XCOPRI may cause problems with the electrical system of the heart (QT shortening). Call your healthcare provider if you have symptoms of QT shortening including fast heartbeat (heart palpitations) that last a long time or fainting.

Suicidal behavior and ideation: Antiepileptic drugs, including XCOPRI, may cause suicidal thoughts or actions in a very small number of people, about 1 in 500. Call your health care provider right away if you have any of the following symptoms, especially if they are new, worse, or worry you: thoughts about suicide or dying; attempting to commit suicide; new or worse depression, anxiety, or irritability; feeling agitated or restless; panic attacks; trouble sleeping (insomnia); acting aggressive; being angry or violent; acting on dangerous impulses; an extreme increase in activity and talking (mania); or other unusual changes in behavior or mood.

Nervous system problems: XCOPRI may cause problems that affect your nervous system. Symptoms of nervous system problems include: dizziness, trouble walking or with coordination, feeling sleepy and tired, trouble concentrating, remembering, and thinking clearly, and vision problems. Do not drive, operate heavy machinery, or do other dangerous activities until you know how XCOPRI affects you .

Do not drink alcohol or take other medicines that can make you sleepy or dizzy while taking XCOPRI without first talking to your healthcare provider.

DISCONTINUATION:

Do not stop taking XCOPRI without first talking to your healthcare provider. Stopping XCOPRI suddenly can cause serious problems. Stopping seizure medicine suddenly in a patient who has epilepsy can cause seizures that will not stop (status epilepticus).

DRUG INTERACTIONS:

XCOPRI may affect the way other medicines work, and other medicines may affect how XCOPRI works. Do not start or stop other medicines without talking to your healthcare provider. Tell healthcare providers about all the medicines you take, including prescription and over-the-counter medicines, vitamins and herbal supplements.

PREGNANCY AND LACTATION:

XCOPRI may cause your birth control medicine to be less effective. Talk to your health care provider about the best birth control method to use.

Talk to your health care provider if you are pregnant or plan to become pregnant. It is not known if XCOPRI will harm your unborn baby. Tell your healthcare provider right away if you become pregnant while taking XCOPRI. You and your healthcare provider will decide if you should take XCOPRI while you are pregnant. If you become pregnant while taking XCOPRI, talk to your healthcare provider about registering with the North American Antiepileptic Drug (NAAED) Pregnancy Registry. The purpose of this registry is to collect information about the safety of antiepileptic medicine during pregnancy. You can enroll in this registry by calling 1-888-233-2334 or go to http://www.aedpregnancyregistry.org .

Talk to your health care provider if you are breastfeeding or plan to breastfeed. It is not known if XCOPRI passes into breastmilk. Talk to your healthcare provider about the best way to feed your baby while taking XCOPRI.

COMMON SIDE EFFECTS:

The most common side effects in patients taking XCOPRI include dizziness, sleepiness, headache, double vision, and feeling tired.

These are not all the possible side effects of XCOPRI. Tell your healthcare provider if you have any side effect that bothers you or that does not go away. For more information, ask your healthcare provider or pharmacist. Call your doctor for medical advice about side effects. You may report side effects to FDA at 1-800-FDA-1088 or at http://www.fda.gov/medwatch .

DRUG ABUSE:

XCOPRI is a federally controlled substance (CV) because it can be abused or lead to dependence. Keep XCOPRI in a safe place to prevent misuse and abuse. Selling or giving away XCOPRI may harm others and is against the law.

INDICATION:

XCOPRI is a prescription medicine used to treat partial-onset seizures in adults 18 years of age and older. It is not known if XCOPRI is safe and effective in children under 18 years of age.

Please see additional patient information in the Medication Guide . This information does not take the place of talking with your healthcare provider about your condition or your treatment.

Please see full Prescribing Information .

About Epilepsy

Epilepsy is the fourth most common neurological disorder. Approximately 3.4 million people are living with epilepsy in the United States , with 150,000 new cases each year in the country. 1,2 Epilepsy is characterized by recurrent, unprovoked seizures. The seizures in epilepsy may be related to a brain injury or a family tendency, but often the cause is completely unknown. Having seizures and epilepsy can affect one's safety, relationships, work, driving, and much more. 3,4 People with epilepsy are at risk for accidents and other health complications, including falling, drowning, depression and sudden unexplained death in epilepsy (SUDEP). 3,4 Despite the availability of many antiepileptic therapies, almost 40 percent of people with epilepsy are not able to achieve seizure freedom, meaning they have epilepsy that remains uncontrolled. 5

About SK Biopharmaceuticals Co., Ltd. and SK Life Science, Inc.

SK Biopharmaceuticals and its U.S. subsidiary SK Life Science are pharmaceutical companies focused on the research, development, and commercialization of treatments for disorders of the central nervous system (CNS) and oncology. In 2017, SK Biopharmaceuticals established a research center to begin its expansion into oncology through research and development efforts. The companies have a pipeline of eight compounds in development in both CNS disorders and oncology. Additionally, SK Biopharmaceuticals is focused on the discovery of new treatments in oncology. For more information, visit SK Biopharmaceuticals' website at http://www.skbp.com/eng and SK Life Science's website at http://www.SKLifeScienceInc.com .

Both SK Biopharmaceuticals and SK Life Science are part of SK Group, one of the largest conglomerates in Korea. SK Inc., the parent company of SK Biopharmaceuticals, continues to enhance its portfolio value by executing long-term investments with a number of competitive subsidiaries in various business areas, including pharmaceuticals and life science, energy and chemicals, information and telecommunication, and semiconductors. In addition, SK Inc. is focused on reinforcing its growth foundations through profitable and practical management based on financial stability, while raising its enterprise value by investing in new future growth businesses.

References

View original content to download multimedia: https://www.prnewswire.com/news-releases/sk-life-science-announces-data-presentations-for-xcopri-cenobamate-tablets-cv-at-the-2024-american-academy-of-neurology-annual-meeting-302110843.html

SOURCE SK Life Science, Inc.

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SK Life Science Announces Data Presentations for XCOPRI (cenobamate tablets) CV at the 2024 American Academy ... - InvestorsObserver

The following is a summary of Lessons for future clinical trials in adults with Becker muscular dystrophy: Disease progression detected by muscle magnetic resonance imaging, clinical and patient-reported outcome measures, published in the March 2024 issue of Neurology by Wel et al.

Researchers started a retrospective study to address the gap in outcome measure evaluation for adult Becker muscular dystrophy (BMD), a disease with variable progression.

They assessed muscle MRI, patient-reported outcomes (PROs), and various clinical measures (Motor Function Measurement (MFM), muscle strength, and timed-function tests) in 21 adults diagnosed with BMD at the beginning of the study and at 9 and 18 months into the follow-up period.

The results showed a significant increase in proton density fat fraction in 10 out of 17 thigh muscles after 9 months and in all thigh and lower leg muscles after 18 months. The 32-item MFM-32 scale showed a decrease of 1.3% (P=0.017), North Star Ambulatory Assessment decreased by 1.3 points (P=0.010), and the patient-reported activity limitations scale deteriorated by 0.3 logits (P=0.018) after 9 months. After 18 months, the 6-minute walk distance decreased by 28.7 meters (P=0.042), 10-meter walking test decreased by 0.1 meters per second (P=0.032), time to climb four stairs test decreased by 0.03 meters per second (P=0.028), and Biodex peak torque measurements of quadriceps decreased by 4.6 Nm (P=0.014) and hamstrings by 5.0 Nm (P=0.019). MFM-32 domain 1 had the highest sensitivity to change, with a standardized response mean of 1.15.

Investigators concluded that whole-thigh PDFF MRI was sensitive to BMD muscle fat changes and that MFM-32 was the most responsive clinical measure.

Source: onlinelibrary.wiley.com/doi/full/10.1111/ene.16282

Here is the original post:
Insights for Future Adult BMD Clinical Trials: Detecting Disease Progression via Muscle MRI, Clinical, and PROs - Physician's Weekly