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"The test results show that the injury is located to the vestibular nerve, which is connected to the semicircular canals in a cavity inside the skull, and which is directly adjacent to the cochlea in the ear. These injuries lead to the inward nerve impulses not working properly, and the brain therefore does not receive important information about body movements and sensory impressions required to maintain a good balance," says Anna Gard, doctoral student at Lund University, resident in neurosurgery at Skåne University Hospital and first author of the study.
Antabuse may help revive vision in people with progressive blinding disorders: Test of drug could prove role of hyperactive retinal cells in blindness, potentially leading to better therapies -- ScienceDaily
A group of scientists led by Richard Kramer, UC Berkeley professor of molecular and cell biology, had previously shown that a chemical -- retinoic acid -- is produced when light-sensing cells in the retina, called rods and cones, gradually die off. This chemical causes hyperactivity in retinal ganglion cells, which ordinarily send visual information to the brain. The hyperactivity interferes with their encoding and transfer of information, obscuring vision.
He realized, however, that the drug disulfiram -- also called Antabuse -- inhibits not only enzymes involved in the body's ability to degrade alcohol, but also enzymes that make retinoic acid. In new experiments, Kramer and collaborator Michael Goard, who directs a lab at UC Santa Barbara (UCSB), discovered that treatment with disulfiram decreased the production of retinoic acid and made nearly-blind mice much better at detecting images displayed on a computer screen.
Wiggling worms suggest link between vitamin B12 and Alzheimer's -- ScienceDaily
"The read-out is black or white -- the worms are either moving or they are not," Tanis said. "When we gave vitamin B12 to the worms that were vitamin B12 deficient, paralysis occurred much more slowly, which immediately told us that B12 was beneficial. The worms with B12 also had higher energy levels and lower oxidative stress in their cells."
Sleep Deprivation Impairs Molecular Clearance From the Brain
One night of sleep deprivation impaired clearance of the tracer substance from most brain regions, including the cerebral cortex, white matter and limbic structures, as demonstrated on the morning of Day 2 after intervention (sleep deprivation/sleep). Moreover, the impaired cerebral clearance in the sleep deprivation group was not compensated by subsequent sleep from Day 2 to 3. The present results provide in vivo evidence that one night of total sleep deprivation impairs molecular clearance from the human brain, and that humans do not catch up on lost sleep.
Damage to white matter is linked to worse cognitive outcomes after brain injury -- ScienceDaily
The most unexpected aspect of our findings was that damage to gray matter hubs of the brain that are really interconnected with other regions didn't really tell us much about how poorly people would do on cognitive tests after brain damage. On the other hand, people with damage to the densest white matter connections did much worse on those tests," explains Justin Reber, PhD, a UI postdoctoral research fellow in psychology and first author on the study. "This is important because both scientists and clinicians often focus almost exclusively on the role of gray matter. This study is a reminder that connections between brain regions might matter just as much as those regions themselves, if not more so."
Brain changes following traumatic brain injury share similarities with Alzheimer's disease: Using MRIs and machine learning, researchers mapped comparable degenerative changes in gray and white matter of the brain -- ScienceDaily
In multiple brain areas of both TBI and Alzheimer's participants, the researchers found reduced cortical thickness when compared to the healthy controls. Cortical thickness is roughly correlated with brain age and its thinning is often associated with reductions in attention, memory and verbal fluency, as well as with decreased ability to make decisions, integrate new information and adapt one's behavior to new situations, among other deficits.
"These findings are the first to suggest that cognitive impairment following a traumatic brain injury is useful for predicting the magnitude of Alzheimer's-like brain degradation," said study author Andrei Irimia, an assistant professor of gerontology, neuroscience and biomedical engineering at the USC Leonard Davis School of Gerontology and the USC Viterbi School of Engineering. "The results may help health professionals to identify TBI victims who are at greater risk for Alzheimer's disease."
Using MRIs, the study identified significant similarities between TBI and Alzheimer's disease in how the brain's gray and white matter degrade after injury. In gray matter -- the part of the brain that contains neuron cell bodies and their short-range connections -- the most extensive similarities were in areas involved in memory (temporal lobes) and decision-making (orbitofrontal cortices).
