Latest Amyloid precursor protein Stories
Amyloid-beta and tau protein deposits in the brain are characteristic features of Alzheimer disease.
Increasing puromycin-sensitive aminopeptidase, the most abundant brain peptidase in mammals, slowed the damaging accumulation of tau proteins that are toxic to nerve cells and eventually lead to the neurofibrillary tangles, a major pathological hallmark of Alzheimer's disease and other forms of dementia.
Like two brothers wrestling fighting who need to be put in separate corners, a pair of protein molecules work together to speed up the toxic events of Alzheimerâ€™s disease.
Misaligned research, medical challenges and harsh economics are thwarting efforts to slow the destructive course of Alzheimer's disease in the United States.
Older adults without dementia and with lower levels in plasma of the biomarkers beta-amyloid 42/40 (protein fragments) had an increased rate of cognitive decline over a period of 9 years.
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.
Study in Mice Indicates Disease's Underlying Causes and Finds Compounds That Normalize the Alzheimer's Brain MORGANTOWN, W.Va., Jan.
The conclusion of a recent experiment provides the foremost evidence for seasonal imprinting of biological clocks in mammals.
A dysfunction in the lining of blood vessels that is linked to cardiovascular illness also appears to play a role in the development of Alzheimerâ€™s disease.
A protein known to exist in the brain for more than 30 years, called 5-lipoxygenase, has been found to play a regulatory role in the formation of the amyloid beta in the brain, the major component of plaques implicated in the development of Alzheimer's disease.
- An armed gangster.