The identification of peripheral neural stem cells could transform the treatment of Parkinson’s disease and spinal cord injuries

Complex neural circuits likely arose independently in birds and mammals, suggesting that vertebrates evolved intelligence multiple times.

More Americans are receiving computed tomography (CT) scans than ever before, and while this technology can save lives, some scientists are concerned about the potential for low doses of ionizing radiation to increase cancer risks.

A study from Tübingen University and the German Center for Diabetes Research reveals that the brain plays a crucial role in obesity and type 2 diabetes development. It shows that even a brief period of consuming high-calorie processed foods can significantly alter brain insulin sensitivity, a key factor in weight gain and metabolic disorders. The research demonstrated that insulin’s appetite-suppressing effect in the brain diminishes after a short-term high-calorie diet, leading to insulin resistance. These effects were observed in healthy participants, suggesting that dietary habits could influence brain function before any significant weight gain occurs. Further research is needed to understand the brain’s role in these conditions.

The number of obese persons has grown significantly in recent decades, which presents significant difficulties for those who are impacted, healthcare systems, and those who provide treatment. The hormone insulin plays a key role in the development of obesity. Up until recently, there have been numerous signs indicating insulin causes neurodegenerative and metabolic disorders, especially in the brain. A recent study by the University Hospital of Tübingen, the German Center for Diabetes Research (DZD), and Helmholtz Munich offers intriguing new insights into the origins of type 2 diabetes and obesity as well as the brain’s function as a critical control center.

Obesity has only been officially recognized as a disease in Germany since 2020, despite the fact that it has long been known to cause a number of illnesses, including diabetes, heart attacks, and even cancer. The World Health Organization has already declared obesity to be an epidemic, affecting over one billion individuals globally and almost 16 million in Germany alone. A body mass index of 30 or more is considered obese, and a poor diet and insufficient exercise are frequently cited as the causes of this chronic illness. However, the mechanisms in the body that lead to obesity and cause the disease are more complex.

Obesity and the role of insulin in the brain

Unhealthy body fat distribution and chronic weight gain are linked to the brain’s sensitivity to insulin. What specific functions does insulin perform in the brain, and how does it affect individuals of normal weight? In their study, Prof. Dr. Stephanie Kullmann and her colleagues at the Tübingen University Hospital for Diabetology, Endocrinology, and Nephrology found the answer to this query. “Our findings demonstrate for the first time that even a brief consumption of highly processed, unhealthy foods (such as chocolate bars and potato chips) causes a significant alteration in the brain of healthy individuals, which may be the initial cause of obesity and type 2 diabetes,” says Prof. Kullmann, the study’s leader. In a healthy state, insulin has an appetite-suppressing effect in the brain. However, in people with obesity in particular, insulin no longer regulates eating behavior properly, resulting in insulin resistance.

The study, “Endothelial TDP-43 Depletion Disrupts Core Blood-Brain Barrier Pathways in Neurodegeneration,” was published on March 14, 2025. The lead author, Omar Moustafa Fathy, an MD/Ph. D. candidate at the Center for Vascular Biology at UConn School of Medicine, conducted the research in the laboratory of senior author Dr. Patrick A. Murphy, associate professor and newly appointed interim director of the Center for Vascular Biology. The study was carried out in collaboration with Dr. Riqiang Yan, a leading expert in Alzheimer’s disease and neurodegeneration research.

This work provides a novel and significant exploration of how vascular dysfunction contributes to neurodegenerative diseases, exemplifying the powerful collaboration between the Center for Vascular Biology and the Department of Neuroscience. While clinical evidence has long suggested that blood-brain barrier (BBB) dysfunction plays a role in neurodegeneration, the specific contribution of endothelial cells remained unclear. The BBB serves as a critical protective barrier, shielding the brain from circulating factors that could cause inflammation and dysfunction. Though multiple cell types contribute to its function, endothelial cells—the inner lining of blood vessels—are its principal component.

“It is often said in the field that ‘we are only as old as our arteries’. Across diseases we are learning the importance of the endothelium. I had no doubt the same would be true in neurodegeneration, but seeing what these cells were doing was a critical first step,” says Murphy.

Omar, Murphy, and their team tackled a key challenge: endothelial cells are rare and difficult to isolate from tissues, making it even harder to analyze the molecular pathways involved in neurodegeneration.

To overcome this, they developed an innovative approach to enrich these cells from frozen tissues stored in a large NIH-sponsored biobank. They then applied inCITE-seq, a cutting-edge method that enables direct measurement of protein-level signaling responses in single cells—marking its first-ever use in human tissues.

This breakthrough led to a striking discovery: endothelial cells from three different neurodegenerative diseases—Alzheimer’s disease (AD), amyotrophic lateral sclerosis (ALS), and frontotemporal dementia (FTD)—shared fundamental similarities that set them apart from the endothelium in healthy aging. A key finding was the depletion of TDP-43, an RNA-binding protein genetically linked to ALS-FTD and commonly disrupted in AD. Until now, research has focused primarily on neurons, but this study highlights a previously unrecognized dysfunction in endothelial cells.

“It’s easy to think of blood vessels as passive pipelines, but our findings challenge that view,” says Omar. “Across multiple neurodegenerative diseases, we see strikingly similar vascular changes, suggesting that the vasculature isn’t just collateral damage—it’s actively shaping disease progression. Recognizing these commonalities opens the door to new therapeutic possibilities that target the vasculature itself.”

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“The findings are significant because they could pave the way for new treatments to keep the brain healthier longer,” says Agustín Ibáñez, a neuroscientist at Trinity College Dublin. “But much more research is needed before these findings can be applied in practice.”

Bryan Johnson took ketamine and monitored his brain activity for 15 days, recording the experience and sharing about it on X.

Johnson is a 47-year-old longevity-obsessed entrepreneur, known for sharing biohacking content across his social media channels. His most recent health experiment involved treatment with the popularized horse tranquilizer.

As he shared in a tweet, he wanted to test what happens to the brain before, during, and after ketamine treatment.

Ketamine has gained popularity as a fast-acting treatment for depression, PTSD, and chronic pain. Unlike traditional antidepressants, it works quickly by targeting the brain’s glutamate system to restore neural connections.

To monitor his brain activity, Johnson used his self-invented Kernel Flow—a form of non-invasive brain interface technology worn on the head.

S brain activity followed fixed, predictable patterns. After, he found his once-rigid thinking to be more flexible, varied, and open to new beliefs or ways of thinking. + Johnson likened his brain on ketamine to a global air traffic network, where each airport—or brain region—has consistent flight routes and traffic volumes.

“After ketamine, my brain’s activity patterns were completely scrambled. Instead of predictable routes between major hubs, traffic was rerouted to smaller, less-used airports across the U.S., Europe, and Asia,” he said in a tweet.

While the trial is limited to members of families with genetic mutations that all but guarantee they will develop Alzheimer’s at a young age, typically in their 30s, 40s or 50s, the researchers expect that the study’s results will inform prevention and treatment efforts for all forms of Alzheimer’s disease.

Called the Primary Prevention Trial, the new study investigates whether remternetug — an investigational antibody being developed by Eli Lilly and Company — can remove plaques of a key Alzheimer’s protein called amyloid beta from the brain or block them from accumulating in the first place. Both genetic and nongenetic forms of Alzheimer’s disease start with amyloid slowly collecting in the brain two decades before memory and thinking problems arise. By clearing out low levels of amyloid beta plaques or preventing them from accumulating during the early, asymptomatic phase of the disease, or both, the researchers hope to interrupt the disease process at the earliest stage and spare people from ever developing symptoms.

“We have seen tremendous progress in the treatment of Alzheimer disease in the past few years,” said Eric McDade, DO, a professor of neurology and the trial’s principal investigator. “Two amyloid-targeting drugs were shown to slow symptoms of the disease and have now been approved by the Food and Drug Administration (FDA) as treatments for people with mild cognitive impairment or mild dementia due to Alzheimer’s disease. This provides strong support for our hypothesis that intervening when amyloid beta plaques are at the very earliest stage, long before symptoms arise, could prevent symptoms from emerging in the first place.”

The trial is part of the Knight Family Dominantly Inherited Alzheimer Network-Trials Unit (Knight Family DIAN-TU), a clinical trials platform designed to find medicines to prevent or treat Alzheimer’s disease. It is closely associated with DIAN, a National Institutes of Health (NIH)-funded international research network led by WashU Medicine that involves research institutes in North America, Australia, Europe, Asia and South America. DIAN follows families with mutations in any of three genes that cause Alzheimer’s at a young age. A child born into such a family has a 50% chance of inheriting such a mutation, and those who do so typically develop signs of dementia near the same age his or her parent did. All the participants in the Primary Prevention Trial come from such families.

“My grandfather passed away from Alzheimer’s, and so did his mother and all but one of his brothers,” said Hannah Richardson, 24, a participant in the Primary Prevention Trial. “My mom and my uncle have been participating in DIAN trials since I was about 10 years old. My mom was always very open about her diagnosis and how it spurred her advocacy for Alzheimer’s research, and I’ve always known I wanted to follow in her footsteps. I am happy to be involved in the Primary Prevention Trial and be involved in research because I know how important it is.”

A recent large-scale study published in Science Advances has revealed a connection between genetic variations associated with dyslexia and structural differences in the brain. These differences were found in areas involved in motor coordination, vision, and language. This provides new insights into the neurological underpinnings of this common learning difficulty.

Dyslexia is a common learning difficulty that primarily affects the skills involved in accurate and fluent word reading and spelling. It’s characterized by challenges with phonological awareness (the ability to recognize and manipulate the sounds in spoken language), verbal memory, and verbal processing speed. People with dyslexia may struggle to decode words, recognize familiar words automatically, and spell words correctly. Importantly, dyslexia is not related to a person’s overall intelligence. It’s considered a neurodevelopmental condition, meaning it arises from differences in how the brain develops and processes information, particularly related to language.

Genetic disposition to dyslexia is associated with brain structure in the general population.

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