Latest Neurofibrillary tangle Stories
Building on research published eight years ago in the journal Chemistry and Biology, Kenneth S. Kosik, Harriman Professor in Neuroscience and co-director of the Neuroscience Research Institute (NRI) at UC Santa Barbara, and his team have now applied their findings to two distinct, well-known mouse models, demonstrating a new potential target in the fight against Alzheimer's and other neurodegenerative diseases.
A new genetically engineered lab rat that has the full array of brain changes associated with Alzheimer's disease supports the idea that increases in a molecule called beta-amyloid in the brain causes the disease.
Goldilocks was on to something when she preferred everything "just right."
Researchers from Boston University School of Medicine (BUSM) have identified a novel group of proteins that accumulate in the brains of patients with Alzheimer's disease.
According to a new study, the neuron-killing pathology of Alzheimer's disease (AD), which begins before clinical symptoms appear, requires the presence of both amyloid-beta (a-beta) plaque deposits and elevated levels of an altered protein called p-tau.
Immunotherapy with the antibody bapineuzumab in patients with mild to moderate Alzheimer disease resulted in decreases in a cerebrospinal fluid biomarker, which may indicate downstream effects on the degenerative process.
Repeated stress triggers the production and accumulation of insoluble tau protein aggregates inside the brain cells of mice.
One of the most distinctive signs of the development of Alzheimer's disease is a change in the behavior of a protein that neuroscientists call tau. In normal brains, tau is present in individual units essential to neuron health.
For decades, researchers have debated whether Alzheimer's disease starts independently in vulnerable brain regions at different times, or if it begins in one region and then spreads to neuroanatomically connected areas.
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