Wednesday, May 24, 2017
A recent scientific study shows that insufficient amount of sleep leads to the development of Alzheimer's disease. Researchers gain more evidence and are beginning to believe that lack and poor quality of sleep results to the fusion of Amyloids, proteins that bond together to form Alzheimer's plaques.
Dr. Maiken Nedergaard, the lead researcher from the University of Rochester Medical Center, explains the glymphatic system that is present in humans. She says that this system is 10 times more active when in slumber than when awake. The process allows cerebrospinal fluid to flow through spaces around the neurons of people's brains. This a method of purging unwanted proteins (Amyloids) and other wastes into the circulatory system garbage collectors and eventually flushes it out of the body.
In simple terms, Nedergaard explains that the brain has its own sanitation and public works department. It is like a network of sewer facilities mostly done during the brain's nightlife. An example of a housekeeping staff descending to building offices for a cleanup duty to avoid the lumping compound that causes Alzheimer's.Read More: Featured in The Science Times: How Alzheimer's Catches People Skimping Sleep: New Study Explains Cause Of Dementia
Introducing the Center for NeuroTherapeutics Discovery
Tuesday, May 16, 2017
The Center for Neural Development and Disease, led by Harris A. (Handy) Gelbard, M.D., Ph.D., since 2008, will now be the Center for NeuroTherapeutics Discovery, reflecting an increased emphasis on translation and the creation of intellectual property that will lead to new therapies for nervous system disorders.
Gelbard, professor of Neurology, Pediatrics, Neuroscience and Microbiology & Immunology, will continue as director. His research, coupled with the work of Charles Thornton, M.D., professor of Neurology and Neuroscience, and Marc Halterman, M.D., Ph.D., associate professor of Neurology, Neuroscience and Pediatrics, will serve as the anchor of the new center. The trio has a strong track record of grants, publications, and patents, as well as academic and commercial relationships that they are actively pursuing to bring new treatments to the public.
“The Center for NeuroTherapeutics Discovery was developed out of the Center for Neural Development and Disease to create more visibility for academic and commercial partnerships as a necessary bridge for bringing new therapeutics forward,” said Gelbard. “This represents a way to do the best and most cutting edge science possible in a time when the traditional avenues towards funding academic research are changing rapidly.”
The center will bring together many investigators from across the Medical Center and River Campus to identify the mechanisms that lead to various neurological disorders, including HIV-associated neurocognitive disorder (Gelbard lab), myotonic dystrophy (Thornton lab) and stroke (Halterman lab). The center remains committed to its members that investigate the molecular signaling events that lead to nervous system disease during development and aging. Industry partnerships and resources will be sought to fast-track existing therapies or create new molecules that affect these disease mechanisms.
Treatments that harness the immune system to help regenerate damaged cells will be a major focus at the center; the team believes that this approach is broadly applicable to a range of acute and chronic neurodegenerative disorders, such as Parkinson’s disease, multiple sclerosis and Alzheimer’s disease.
Monday, January 30, 2017
Major Step toward Longer-Lasting HIV Treatment
A drug developed at the University of Rochester Medical Center extends the effectiveness of multiple HIV therapies by unleashing a cell’s own protective machinery on the virus. The finding, published today in the Journal of Clinical Investigation, is an important step toward the creation of long-acting HIV drugs that could be administered once or twice per year, in contrast to current HIV treatments that must be taken daily.
The drug, called URMC-099, was developed in the laboratory of UR scientist Harris A. (“Handy”) Gelbard, M.D., Ph.D. When combined with “nanoformulated” versions of two commonly used anti-HIV drugs (also called antiretroviral drugs), URMC-099 lifts the brakes on a process called autophagy.
Normally, autophagy allows cells to get rid of intracellular “trash,” including invading viruses. In HIV infection, the virus prevents cells from turning on autophagy; one of the many tricks it uses to survive. When the brake on autophagy is lifted, cells are able to digest any virus that remains after treatment with antiretroviral therapy, leaving cells free of virus for extended periods of time.
Harris A. (“Handy”) Gelbard, M.D., Ph.D.
“This study shows that URMC-099 has the potential to reduce the frequency of HIV therapy, which would eliminate the burden of daily treatment, greatly increase compliance and help people better manage the disease,” said Gelbard, professor and director of UR’s Center for Neural Development and Disease, who has studied HIV/AIDS for the past 25 years. The finding builds on previous research that Gelbard conducted with Howard E. Gendelman, M.D., professor and chair of the Department of Pharmacology/Experimental Neuroscience at the University of Nebraska Medical Center.Read More: URMC Drug Extends Effectiveness of HIV Therapy