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Alzheimer's first substantive description of plaques appeared in 1911. [11] In contrast, Oskar Fischer published a series of comprehensive investigations of plaques and dementia in 1907, 1910 and 1912. [11] By 1911, Max Bielschowsky proposed the amyloid-nature of plaque deposits.
The biochemistry of Alzheimer's disease, the most common cause of dementia, is not yet very well understood. Alzheimer's disease (AD) has been identified as a proteopathy: a protein misfolding disease due to the accumulation of abnormally folded amyloid beta (Aβ) protein in the brain. [1]
Amyloid beta (Aβ, Abeta or beta-amyloid) denotes peptides of 36–43 amino acids that are the main component of the amyloid plaques found in the brains of people with Alzheimer's disease. [2] The peptides derive from the amyloid-beta precursor protein (APP), which is cleaved by beta secretase and gamma secretase to yield Aβ in a cholesterol ...
A main theory behind the cause of Alzheimer’s disease is the build-up of the protein amyloid-beta in the brain. Researchers from the University of Cincinnati provide evidence suggesting it’s ...
New research is contradicting previously held views that only neurons secret beta-amyloid that forms toxic plaques, a marker of Alzheimer's disease in the brain. The study points to another ...
New preclinical-stage research suggests that targeting a specific protein in the brain could help clear toxic amyloid plaques typically linked to Alzheimer's disease progression.
Amyloid plaque Aβ protein species ends in residue 40 or 42, [4] but it is suspected that Aβ42 form is crucial in the pathogenesis of AD. Although Aβ42 makes up less than 10% of total Aβ, it aggregates at much faster rates than Aβ40. [5] Aβ42 is the initial and major component of amyloid plaque deposits.
The cause for most Alzheimer's cases is still mostly unknown, [14] except for 1–2% of cases where deterministic genetic differences have been identified. [17] Several competing hypotheses attempt to explain the underlying cause; the most predominant hypothesis is the amyloid beta (Aβ) hypothesis. [14]
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