Having disrupted sleep leads to increase in brain proteins associated with Alzheimer's disease, results of a study showed Monday. "We were not surprised to find that tau levels didn't budge after just one night of disrupted sleep while amyloid levels did, because amyloid levels normally change more quickly than tau levels," Yo-El Ju, assistant professor of neurology and the lead study author, said in a statement. "I think that may lead to chronically elevated amyloid levels, which animal studies have shown lead to increased risk of amyloid plaques and Alzheimer's." "As Alzheimer's disease progresses, caregiving becomes very important," Christopher Taylor, a CDC epidemiologist who led the study team, told the news outlet at the time.
PARIS – Scientists have used flickering LED lights to shrink, in mouse brains, the beta amyloid plaques associated with Alzheimer's Disease in humans, they reported on Wednesday. While too early to say if this could translate into a much-needed treatment for the debilitating illness, it does present a promising avenue for further research, said the team -- some of whom have started a company to do just that. "It's a big'if,' " said Li-Huei Tsai of the Massachusetts Institute of Technology, who co-authored the study. "But if humans behave similarly to mice in response to this treatment, I would say the potential is just enormous, because it is so non-invasive and it's so accessible." She underlined that many therapies shown to work in mice in the past have failed in humans.
Another one bites the dust. Pharmaceutical giant Merck has halted a trial of a promising Alzheimer's drug, verubecestat, after it was determined that there was virtually no chance of it working. This comes just two months after the failure of another Alzheimer's drug, solanezumab. Both drugs target beta amyloid plaque, the sticky gunk that accumulates in the brains of people with the disease. These failures have revived doubts over the long-held theory that beta amyloid is crucial in causing the disease.
Now more than ever, Alzheimer's disease poses an enormous burden. The neurodegenerative disease afflicts more than five million Americans, robbing them of their memories and placing strain and heartache on their loved ones. This toll costs the U.S. economy hundreds of billions of dollars each year. But a new study of mice published in the Journal of Experimental Medicine suggests that by shutting off just one protein, future medications could potentially break up the sticky plaques associated with Alzheimer's. The protein in question, BACE1, plays a fundamental role in neural development.
The root cause of Alzheimer's, a progressive disease that as of 2013 affects some 5 million Americans, is still not completely understood. Researchers know that hallmarks of the disease are tiny balls of plaque that accumulate in Alzheimer's patients' brains. But how and why they form was still pretty much a mystery. Now, researchers at Harvard University, made a surprising finding: Proteins in the brain leftover from fighting off common infections like from a virus or a bacteria, clump together and create the plaque that is ubiquitously found in Alzheimer's patients. The new research, published yesterday in the journal Science, could pave the way to more precise research on how to stop or prevent the disease.