Latest Neurofibrillary tangle Stories
In one of the first studies of its kind, UCLA researchers used a unique brain scan to assess the levels of amyloid plaques and neurofibrillary tangles â€” the hallmarks of Alzheimer's disease â€” in adults with Down syndrome.
Researchers using two brain-imaging technologies have found that apparently normal older individuals with brain deposits of amyloid beta â€“ the primary constituent of the plaques found in the brains of Alzheimer's disease patients â€“ also had changes in brain structure similar to those seen in Alzheimer's patients.
Amyloid-beta and tau protein deposits in the brain are characteristic features of Alzheimer disease.
A Blanchette Rockefeller Neurosciences Institute (BRNI) study published today in the Journal of Neuroscience reveals underlying causes for the degeneration of synapses in Alzheimer's Disease and identifies promising pharmaceutical solutions for the devastating condition that affects more than 5 million people in the United States.
Dynamic regulation of the chaperone protein Hsp27 was required to get rid of abnormally accumulating tau in the brains of mice genetically modified to develop the memory-choking tau tangles associated with Alzheimer's disease, a University of South Florida-led study found.
Research from the Laboratory of Psychiatry and Experimental Alzheimers Research (http://www2.i-med.ac.at/psychlab/) at the Medical University Innsbruck (Austria) demonstrated that chronic high fat cholesterol diet in rats exhibited pathologies similar to Alzheimer's disease.
A new study uncovers a protein modification that may contribute to the formation of neuron-damaging neurofibrillary tangles in the human brain.
An international team of Alzheimerâ€™s disease experts, led by Washington University School of Medicine in St. Louis, has uncovered a gene variation that appears to predict the rate at which Alzheimerâ€™s disease will progress.
- Two Target Tau; Two May Reduce Tau Though Their Target Was Amyloid - HONOLULU, July 13 /PRNewswire-USNewswire/ -- The primary therapeutic target in Alzheimer's disease has been the beta amyloid peptide, which clusters outside cells in the brain to form sticky clumps known as plaques.
TGen-led team finds 3 proteins that dismantle 'bridges' within brain cells.
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