#neuronal-dna-repair

#neuronal-dna-repair

DNA damage can originate from internal sources like metabolic by-products or normal cellular activities, as well as external factors such as cosmic radiation, diet, and pollution.

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.

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.

Tumours lure and then hijack nearby sensory neurons to boost their own growth. The cancer cells use these neurons to send a signal to the brain that subdues the activity of immune cells around the tumour, which allows it to grow unchecked. When researchers deactivated these neurons in mice with lung cancer, they saw "a huge, dramatic reduction" in tumour growth - more than 50% - says cancer immunologist and study co-author Chengcheng Jin.

Young, two-month-old lab mice housed with older, 18-month-old mice showed really impaired cognition. Researchers exposed young mice raised in a sterile, microbe-free environment to gut bacteria from old mice, causing the younger animals to perform worse on cognitive tests, as if they had prematurely aged, just like the cohoused mice.

In the originally published version of this article, Extended Data Fig. 4 contained inadvertent duplications introduced during figure assembly: panel 4c (the bottom of the second column) erroneously reused images from panel 4a (the bottom of the third column); panel 4c (the upper panel of the third column) erroneously reused images from panel 4a (the upper panel of the rightmost column);

We've always said that SuperAgers show that the aging brain can be biologically active, adaptable, flexible, but we didn't know why. This is biological proof that their brains are more plastic, and a real discovery that shows that neurogenesis of young neurons in the hippocampus may be a contributing factor.

N-methyl-d-aspartate receptors (NMDARs) are glutamate-gated ion channels that mediate excitatory neurotransmission throughout the brain1. As obligate heterotetramers, their activation requires the binding of both glycine and glutamate2. Although recent structural studies have provided insights into endogenous receptors from select brain regions3, most previous work has relied on recombinant receptors and engineered constructs, which limits our understanding of native NMDARs across the whole brain.

For decades, scientists have observed a consistent pattern: women typically live about five years longer than men and exhibit slower cognitive decline as they age. Now, groundbreaking research from the University of California, San Francisco has uncovered a surprising biological mechanism that may explain this disparity. The discovery centers on what researchers once dismissed as a dormant structure, the so-called "silent" X chromosome that exists in every female cell.

For years, scientists have viewed cancer as a localized glitch in which cells refuse to stop dividing. But a new study suggests that, in certain organs, tumors actively communicate with the brain to trick it into protecting them. Scientists have long known that nerves grow into some tumors and that tumors containing lots of nerves usually lead to a worse prognosis.

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.