Researchers have identified a genetic region, HAR123, that may help explain what makes the human brain unique.
Category: neuroscience – Page 111
Scientists discover brain layers that get stronger with age
Researchers have discovered that parts of the human brain age more slowly than previously thought—particularly in the region that processes touch. By using ultra-high-resolution brain scans, they found that while some layers of the cerebral cortex thin with age, others remain stable or even grow thicker, suggesting remarkable adaptability. This layered resilience could explain why certain skills endure into old age, while others fade, and even reveals built-in compensatory mechanisms that help preserve function.
Novel protein therapy shows promise as first-ever antidote for carbon monoxide poisoning
University of Maryland School of Medicine (UMSOM) researchers, along with their colleagues, engineered a new molecule that appears promising as an effective antidote for carbon monoxide poisoning with fewer side effects than other molecules currently being tested, according to a new study published in the journal PNAS.
Carbon monoxide poisoning accounts for 50,000 emergency room visits in the U.S. each year and causes about 1,500 deaths. These deaths may occur when carbon monoxide released from combustion builds up in an enclosed space, which can result from ventilation failures in indoor natural gas burning equipment, or running gasoline generators or automobiles indoors or in a closed garage. Carbon monoxide poisoning is also associated with most fires from smoke inhalation.
Currently, the only treatments for carbon monoxide poisoning are oxygen-based therapies, which help the body eliminate the toxic gas. However, even with treatment, nearly half of survivors suffer long-term heart and brain damage. This has created an urgent need for faster, more effective therapies.
Neural navigation: Engineers map brain’s smallest blood vessels using computer models
Healthy brain function relies on a steady supply of blood. Disruptions in blood flow are linked to major neurological conditions like stroke, Alzheimer’s disease (AD), and traumatic brain injuries. But understanding how the brain fine-tunes this flow—especially across its smallest blood vessels—remains a challenge.
The brain’s blood supply includes a vast network of vessels, ranging from large arteries to microscopic capillaries. Between these lie transitional zone (TZ) vessels—such as penetrating arterioles, precapillary arterioles, and capillary sphincters—that bridge the gap and may play a big role in regulating flow. But their exact contribution, particularly during increased brain activity, remains a subject of scientific debate.
To explore these dynamics, researchers from the College of Engineering and Computer Science at Florida Atlantic University and the FAU Sensing Institute (I-SENSE) developed a highly detailed computer model of the mouse brain’s vasculature, treating each vessel segment as a tiny, adjustable valve.
Molecular mechanisms show how the blood-brain barrier gets leakier with age
A new study from researchers at the University of Illinois Chicago reveals how the blood-brain barrier gets leakier with age, contributing to memory deficits. The study, published in Cell Reports, uncovered the molecular mechanisms behind this process and could provide new therapeutic targets to address cognitive decline earlier in the aging process.
The blood-brain barrier is a layer of cells lining the brain’s blood vessels that keep viruses, bacteria and toxins out while allowing helpful nutrients and chemicals in. A key structure of the blood-brain barrier are tight junctions that act as bridges between cells, restricting entry of molecules. A protein called occludin helps fulfill this essential role.
“It’s a highly regulatable process that allows some molecules to go through and others to remain in circulation,” said Yulia Komarova, UIC associate professor in the department of pharmacology and regenerative medicine at the College of Medicine and senior author of the study. “Basically, it’s a mechanism that separates the central nervous system from everything else.”
New Study Suggests Cancer Drug Could Be Used to Target Protein Connection That Spurs Parkinson’s Disease
In studies with genetically engineered mice, Johns Hopkins Medicine researchers say they have identified a potentially new biological target involving Aplp1, a cell surface protein that drives the spread of Parkinson’s disease-causing alpha-synuclein.
The findings, published May 31 2024 in Nature Communications, reveal how Aplp1 connects with Lag3, another cell surface receptor, in a key part of a process that helps spread harmful alpha-synuclein proteins to brain cells. Those protein buildups are hallmarks of Parkinson’s disease.
Notably, the researchers say, Lag3 is already the target of a combination cancer drug approved by the U.S. Food and Drug Administration (FDA) that uses antibodies to “teach” the human immune system what to seek and destroy.