According to British neurologists, COVID-19 can cause serious damage to the brain and central nervous system. Such damage can lead to psychosis, paralysis and strokes, which are often detected in their late stages.
Category: neuroscience – Page 751
Biologists from the University of Bayreuth have discovered a uniquely rapid form of regeneration in injured neurons and their function in the central nervous system of zebrafish. They studies the Mauthner cells, which are solely responsible for the escape behavior of the fish, and previously regarded as incapable of regeneration. However, their ability to regenerate crucially depends on the location of the injury. In central nervous systems of other animal species, such a comprehensive regeneration of neurons has not yet been proven beyond doubt. The scientists report their findings in the journal Communications Biology.
Mauthner cells are the largest cells found in animal brains. They are part of the central nervous system of most fish and amphibian species and trigger life-saving escape responses when predators approach. The transmission of signals in Mauthner cells to their motoneurons is only guaranteed if a certain part of these cells, the axon, is intact. The axon is an elongated structure that borders the cell body with its cell nucleus at one of its two ends. If the injury of the axon occurs close to the cell body, the Mauthner cell dies. If the axon is damaged at its opposite end, lost functions are either not restored at all or only slowly and to a limited extent. However, the Mauthner cell reacts to an injury in the middle of the axon with rapid and complete regeneration. Indeed, within a week after the injury, the axon and its function are fully restored, and the fish is able to escape approaching predators again.
“Such a rapid regeneration of a neuron was never observed anywhere in the central nervous system of other animal species until now. Here, regeneration processes usually extend over several weeks or months,” says Dr. Alexander Hecker, first author of the new study and member of the Department of Animal Physiology. This finding clearly disproves the widely accepted view in the scientific community that Mauthner cells are unable to regenerate.
The brain-computer linkup firm, Neuralink, is set to reveal more about its progress toward its goals.
A little-studied liver protein may be responsible for the well-known benefits of exercise on the aging brain, according to a new study in mice by scientists in the UC San Francisco Eli and Edythe Broad Center for Regeneration Medicine and Stem Cell Research. The findings could lead to new therapies to confer the neuroprotective effects of physical activity on people who are unable to exercise due to physical limitations.
Exercise is one of the best-studied and most powerful ways of protecting the brain from age-related cognitive decline and has been shown to improve cognition in individuals at risk of neurodegenerative disease such as Alzheimer’s disease and frontotemporal dementia —even those with rare gene variants that inevitably lead to dementia.
But many older adults are not able to exercise regularly due to physical limitations or disabilities, and researchers have long searched for therapies that could confer some of the same neurological benefits in people with low physical activity levels.
Study could lead to a pill that confers the benefits of physical activity on cognition.
When trying to complete a task we are constantly bombarded by distracting stimuli. How does the brain filter out these distractions and enable us to focus on the task at hand? Psychologists at the University of California, Riverside, have made a discovery that could lead to an answer.
Experimenting on mice, they located the precise spot in the brain where distracting stimuli are blocked. The blocking disables the brain from processing these stimuli, which allows concentration on a particular task to proceed.
Edward Zagha, an assistant professor of psychology, and his team trained mice in a sensory detection task with target and distractor stimuli. The mice learned to respond to rapid stimuli in the target field and ignore identical stimuli in the opposite distractor field. The team used a novel imaging technique, which allows for high spatiotemporal resolution with a cortex-wide field of view, to find where in the brain the distractor stimuli are blocked, resulting in no further signal transmission within the cortex and, therefore, no triggering of a motor response.
UK neurologists publish details of mildly affected or recovering Covid-19 patients with serious or potentially fatal brain conditions.
Look deep inside our cells, and you’ll find that each has an identical genome –a complete set of genes that provides the instructions for our cells’ form and function.
But if each blueprint is identical, why does an eye cell look and act differently than a skin cell or brain cell? How does a stem cell—the raw material with which our organ and tissue cells are made—know what to become?
In a study published July 8, University of Colorado Boulder researchers come one step closer to answering that fundamental question, concluding that the molecular messenger RNA (ribonucleic acid) plays an indispensable role in cell differentiation, serving as a bridge between our genes and the so-called “epigenetic” machinery that turns them on and off.
Having hypertension in midlife (ages 40 through 60) is associated with elevated risk of cognitive impairment and Alzheimer’s dementia later in life, even more so than having the so-called Alzheimer’s gene.
“It is clear that cerebral vascular disease”—that is, hardening of the arteries inside our brain—“and cognitive decline travel hand in hand,” something I’ve addressed before. “However, the independent association of AD [Alzheimer’s disease] with multiple AVD [atherosclerotic vascular disease] risk factors suggests that cholesterol is not the sole culprit in dementia.”
As I discuss in my video Higher Blood Pressure May Lead to Brain Shrinkage, one of the most consistent findings is that elevated levels of blood pressure in midlife, ages 40 through 60, is associated with elevated risk of cognitive impairment and Alzheimer’s dementia later in life—in fact, even more so than having the so-called Alzheimer’s gene.