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Parkinson’s medication shows promise in treating treatment-resistant depression

For many people who suffer from depression, the condition is not just about feeling down but also about a loss of motivation and difficulty finding pleasure in activities they used to enjoy. A new study conducted in Sweden shows that a medicine used to treat Parkinson’s disease can be used as an add-on therapy to alleviate these symptoms in some patients with treatment-resistant depression. The study has been published in Nature Medicine.

The researchers at Lund University and the psychiatric services in Region Skåne have identified the potential new therapy for the condition associated with depression that involves a reduced ability to feel joy, pleasure or motivation—known as anhedonia. Those affected may lose interest in things that they previously found meaningful or rewarding.

The study is an example of what is known as drug repurposing, whereby an already approved medicine is used to treat a different condition. In this study, the researchers investigated pramipexole, which has long been used to treat Parkinson’s disease, as an add-on therapy for depression with marked anhedonia.

Popular joint pain supplement might increase Alzheimer’s risk, study says

A popular over-the-counter supplement taken for joint pain might increase people’s risk for Alzheimer’s disease, a new study says.

Glucosamine use is associated with a 25% higher odds that a person will progress from mild cognitive impairment to dementia and Alzheimer’s disease, researchers report in the journal Nature Metabolism.

“While it’s an association and not proof of causality, it does raise an important clinical question that now deserves much more attention,” researcher Matt Gentry said in a news release. He’s chair of biochemistry and molecular biology at the University of Florida.

Faulty protein cleanup gene tied to severe early-onset neurological disorders

Though protein clumps associated with Alzheimer’s and Parkinson’s were discovered more than a century ago, researchers remain largely unable to prevent them from forming or eliminate them from the brain. And though a variety of therapies have taken aim at tau tangles, beta-amyloid plaques and Lewy bodies, among other notorious aggregates, none have been very effective at stopping disease progression.

Rockefeller’s Hermann Steller and his team in the Strang Laboratory of Apoptosis and Cancer Biology have long been focused on understanding how the cell’s protein-degrading machines, called proteasomes, are regulated. His lab discovered that a transporter protein termed PI31 shuttles proteasomes over long distances from the nerve cell body to synapses. When this system fails, synapses become depleted of degradative capacity, and proteins that should have been eliminated accumulate. As a result, synaptic communication breaks down, protein clumps form and neuronal health deteriorates.

Now a new study in Nature Communications, led by researchers from University College London and contributed to by Steller’s lab, has identified mutations in PSMF1, the gene that produces PI31, that cause the protein to malfunction. Moreover, the scientists demonstrated that these mutations cause a spectrum of severe, very early-onset neurological disorders.

A Supplement For Joint Pain Could Accelerate Alzheimer’s Memory Loss

People with Alzheimer’s disease who took the common supplement glucosamine were 25% more likely to die within five years than those who didn’t.

That’s the key finding of a new study that my colleagues and I published in the journal Nature Metabolism.

Glucosamine is a sugar molecule that’s sold over the counter as a remedy for joint pain and arthritis. More than 40 million Americans take it each year.

Biohybrid: The Science biohybrid architecture integrates neurons into its electronics, rather than trying to integrate electronics into the brain

Using hundreds of thousands of neurons anchored to the device, the Science architecture connects to the brain with orders of magnitude more bandwidth than current state-of-the-art devices, while avoiding the damage and limitations of putting wires into a brain.

Biohybrid Brain–Machine Interfaces: The Next Evolution of Human Intelligence

Brain–machine interfaces (BMIs) are no longer just science fiction; they are the gateway to a future where thought itself can interact directly with technology. These systems read the brain’s electrical activity and, in turn, stimulate neurons — forming a two-way communication link between biology and machines.

In just a few decades, BMIs have evolved from laboratory curiosities into one of the fastest-growing frontiers in science and engineering. The possibilities are staggering. In the future, neural interfaces could restore vision to the blind, enable paralyzed individuals to move again, facilitate seamless communication between human brains and artificial intelligence, and ultimately power virtual realities that are indistinguishable from the physical world.

This convergence of biology, computing, and neuroscience marks the dawn of a new era — one where the boundaries between human and machine begin to blur.

Gut microbes unlock hormone signaling that regulates gut movement, study suggests

Millions of people worldwide are periodically or chronically affected by gut-related conditions, such as irritable bowel syndrome (IBS), gastroesophageal reflux disease (GERD) and gastroenteritis. Uncovering the physiological and biological processes that contribute to gut health could thus be highly valuable, as it might help devise more effective interventions to prevent and treat these ailments.

The transit of food, fluids and waste through the intestine is known to be coordinated by various interacting systems in the body, including gut wall muscles, neurons in the gastrointestinal tract and hormones. A growing body of research has also been exploring the crucial contribution of bacteria and other microorganisms residing in the digestive tract, which are collectively referred to as the gut microbiome.

Researchers at Boston Children’s Hospital, Harvard Medical School, the University of North Carolina at Chapel Hill and Laval University recently carried out a study aimed at better understanding how these gut microbes interact with specific sex hormones and nerve cells that control the movement of muscles in the intestines.

Researchers identify brain ‘entrapment’ patterns associated with depression

Researchers at the Icahn School of Medicine at Mount Sinai have identified distinctive patterns in how the brain transitions between activity states in people with depression, providing new insight into why depressive symptoms can feel persistent and difficult to overcome.

Published online in Nature Communications, the study combined advanced neuroimaging techniques with mathematical modeling to examine how the brain moves between functional activity states over time. The findings suggest that depression may involve a form of “brain-state entrapment,” in which the brain becomes more likely to enter certain patterns of activity and less likely to transition out of them.

“Many patients describe depression as feeling stuck in negative patterns of thought, mood and behavior,” said Yael Jacob, Ph.D., assistant professor of psychiatry at the Dennis S. Charney, MD, Depression and Anxiety Discovery Center at the Icahn School of Medicine at Mount Sinai and senior author of the paper. “Our findings suggest that this experience of being ‘stuck’ may reflect measurable changes in the brain’s underlying dynamics.”

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