#corticobasal-degeneration

#corticobasal-degeneration

Lewy body dementia (LBD) is the second-most-common neurodegenerative cause of dementia, after Alzheimer's Disease. But it's the most-common cause that doesn't receive sufficient attention.

This could open up some interesting possibilities for therapeutic interventions for depression-like behaviors or maladaptive changes in motivational behaviors down the road where microglia are known to play a really important role.

Anyone living with schizophrenia understands the true limitations of current treatment options. Antipsychotics remain the single leading treatment for the disorder, and they are riddled with undesirable side effects. Weight gain, tardive dyskinesia, and excessive drowsiness are a few. Much research is devoted to expanding the range of medication options, and few academics have pursued other avenues. However, there is a possibility that treatment for schizophrenia can be approached through cellular methods if long-term research validates early signs of hope.

A groundbreaking study found that adults who sit for 10 or more hours daily face a significantly higher risk of dementia compared to those who sit less. The research, which tracked over 50,000 adults using wearable devices, revealed that the risk increases dramatically after crossing that 10-hour threshold.

According to University of Michigan neuroscientists, not only can their AI vision language model diagnose neurological disorders from MRI scans with high performance accuracy, but it also has foundation model capabilities, making it a flexible, general-purpose solution that can be tailored for a wide variety of medical imaging. "These results demonstrate that Prima has foundation model properties, and reported performance will continue to improve with additional health system training data and larger compute budgets," wrote the study's authors in the preprint.

Artificial intelligence (AI) machine learning is making a difference in assistive technology to help restore movement for the paralyzed. A new study in the American Institute of Physics journal APL Bioengineering shows how AI has the potential to restore lower-limb functions in those with severe spinal cord injuries (SCIs) by identifying patterns in brain signals captured noninvasively via electroencephalography (EEG).

Most people will forget a name, misplace their phone, or lose track of a conversation at some point. Usually, those moments pass without much thought. But for many adults, especially as they age, small lapses can trigger a much deeper fear: Is this the beginning of cognitive decline? As a neurologist, I hear this concern often. And as a researcher, I have learned something important: Worry about cognition and cognitive disease are not the same thing.

Before treatment began, participants underwent neuroimaging. Instead of relying on a single modality, the researchers fused structural connectivity (how regions are physically wired) with functional connectivity (how regions co-activate at rest). The goal was not to throw every possible feature at a black box, but to learn a constrained pattern-what the authors call structure-function "covariation"-that carries the most predictive signal for outcome. In other words, the model tries to find the smallest set of connections that meaningfully forecasts symptom change.

Decades of research show that people who have more years of education, more cognitively demanding jobs or more mentally stimulating hobbies all tend to have a reduced risk of cognitive impairment as they get older. Experts think this is partly thanks to cognitive reserve: Basically, the more brain power you've built up over the years, the more you can stand to lose before you experience impairment.

Haavik was surprised to hear this because the scientific data do not suggest an unequivocal link between low levels of the neurotransmitter dopamine and ADHD. But the idea that low dopamine is a direct cause of ADHD is a common misconception, one that's amplified on social media and even in popular books about the condition. The reality, Haavik and other researchers say, is that the causes of ADHD are more diverse and nuanced than a simple deficit in one chemical cue in the brain.

But questions remain about the accuracy and uncertainty of these tests, and experts caution that the assays aren't ready for prime time. While the results here are encouraging, they are not yet at the level of having significant clinical benefit for individual patients, says Corey Bolton, a clinical neuropsychologist and an assistant professor of medicine at Vanderbilt University Medical Center, who was not involved in the new study.

New therapies for Alzheimer's disease should target a particular gene linked to the condition, according to researchers who said most cases would never arise if its harmful effects were neutralised. The call to action follows the arrival of the first wave of drugs that aim to treat Alzheimer's patients by removing toxic proteins from the brain. While the drugs slow the disease down, the benefits are minor,

When a person suffers a stroke, physicians must restore blood flow to the brain as quickly as possible to save their life. But, ironically, that life-saving rush of blood can also trigger a second wave of damage - killing brain cells, fueling inflammation and increasing the odds of long-term disability. Now, in a study published in the journal Neurotherapeutics, Northwestern University scientists have developed an injectable regenerative nanomaterial that helps protect the brain during this vulnerable window.

To make their discovery, researchers examined donated eye tissue from more than 100 people who had died with Alzheimer's, mild cognitive impairment or no signs of dementia. They were looking specifically for C. pneumoniae, because previous research has already linked it to Alzheimer's. The bacteria has also been detected in brain tissue from patients who died with the condition, sometimes found close to the sticky amyloid plaques and tangles believed to drive memory loss and confusion.

You know that moment when you walk into a room and completely forget why you went there? Or when someone you've known for years walks up to you at the grocery store and their name just... vanishes from your brain? Last week, I spent ten minutes searching for my reading glasses while they were sitting on top of my head. My first thought wasn't "oh, silly me." It was "Is this how it starts?"

Remember when you first noticed your parents' hands trembling slightly as they poured coffee or signed a check? I started paying attention after my mother mentioned it during one of our Sunday calls, brushing it off as "just getting older." But that conversation sent me down a research rabbit hole that revealed something fascinating: those tiny tremors that appear after 60 aren't always what they seem, and knowing the difference between normal aging and something more serious could change everything.

Researchers used data from two health studies to track the caffeine-drinking habits of more than 130,000 people over four decades. They found that drinking 2-3 cups of coffee or 1-2 cups of tea a day was associated with the greatest reductions in rate of cognitive decline, a result that held true even in people with a genetic variant called APOE4, which is associated with Alzheimer's disease.