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.
In a paper just published in the prestigious journal Neuron, Harvard Medical School/Mass General Hospital Geneticist Dr. Rudy Tanzi, together with lead author, Dr. Jaehong Suh and their team, identified two rare mutations in the human gene called "ADAM10" that lead to the most common, late-onset variant of Alzheimer's. Tanzi's research suggests that the ADAM10 gene makes an enzyme called alpha-secretase, which cleaves the Amyloid Precursor Protein (APP) to prevent the formation of beta-amyloid, the toxic protein that triggers brain pathology in Alzheimer's disease.
For several years now, researchers have been aware of important links between cholesterol and Alzheimer's disease. A new study by Dr. Dora Kovacs and her team at Massachusetts General Hospital brings us one step closer to a potential drug that could interrupt the disease process.
An innovative new public/private collaboration between Cure Alzheimer’s Fund and the National Institute of Mental Health (NIMH) already has started to bear fruit.
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.
Research uncovering 12 new gene variations connected to the cause of the early-onset familial form of Alzheimer’s disease (EO-FAD), which generally strikes before the age of 65, is being published in the journal Molecular Psychiatry.
While many were anxious to accept initial findings showing a drug known as Targretin’s “too good to be true” lab results with Alzheimer’s disease, subsequent attempts to confirm and replicate the original data regarding the ability of Targretin to remove amyloid plaques, the cardinal lesion of the disease, have largely failed. Cure Alzheimer’s Fund Research Consortium members Dr. Sangram Sisodia, professor of neuroscience at the University of Chicago and Dr.
BOSTON— Excessive levels of the protein CD33 can impede the clearance of the plaque-forming protein, amyloid beta, the key component of senile plaques in the brains of Alzheimer’s disease patients. The discovery, made by Dr. Rudolph Tanzi and colleagues at Massachusetts General Hospital, and co-funded by the Cure Alzheimer’s Fund and the National Institute of Mental Health (NIMH) will be published in the journal Neuron.
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.
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.
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