Posted: Dec. 19, 2013
Brain aging is associated with lower production of circadian clock proteins, which synchronize biological processes to light and dark cycles. In Alzheimer’s and other neurodegenerative diseases, circadian dysfunction is commonly observed.
Posted: Jul. 1, 2013
BOSTON – New research examining levels of the hallmark proteins linked to Alzheimer's disease found in patients suffering from post-operative cognitive changes (POCC) may lead to safer surgery care and better post-operative outcomes for senior adults.
Posted: Apr. 14, 2013
The study, led by Cure Alzheimer’s Research Consortium member Sam Gandy, M.D., Ph.D., of the Icahn School of Medicine at Mount Sinai, examined how elements in air pollution such as nickel nanoparticles affect the levels of certain peptides in the brain that are found to be at heightened levels in patients suffering from Alzheimer’s Disease.
“We don’t yet completely understand why the peptides accumulate, but we do know the genes responding to the peptides play an important role in developing Alzheimer’s,” said Gandy.
Posted: Apr. 11, 2013
Traumatic Brain Injury (TBI) can lead to neurodegenerative syndromes that include Alzheimer's Disease (AD) and Chronic Traumatic Encephalopathy (CTE).
The April issue of Nature Reviews Neurology is devoted to Traumatic Brain Injury (TBI) and Chronic Traumatic Encephalopathy (CTE). Cure Alzheimer’s Fund research consortium member, Sam Gandy, M.D., Ph.D., of the Icahn School of Medicine at Mount Sinai is senior author of the lead review and overview.
Posted: Jan. 23, 2013
Meet Dr. Giuseppina Tesco, Cure Alzheimer’s Funded researcher, and assistant professor of neuroscience, Alzheimer’s Disease Research Laboratory, Department of Neuroscience, Tufts University School of Medicine.
Posted: Nov. 11, 2012
Consensus among Alzheimer’s researchers about the origins of the disease is growing. Most, including members of Cure Alzheimer’s Fund Research Consortium, agree that a combination of factors, beginning with the excessive build-up of the peptide Abeta42 triggering the development of tau tangles, nerve cell death, and inflammation are all required for Alzheimer’s pathology.
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