Alzheimer's Culprit is Beta-Amyloid Plaque
1. Beta amyloid is a protein that is made by cells during normal metabolism. But in AD, there is an abnormal cleavage of this protein in the cell membrane. 2.Beta amyloid can bind to dendrites on nerves and interfere with their normal function. 3.Smaller beta amyloid proteins accumulate to form large plaques between nerve cells.
Amyloid-beta (Aβ or Abeta) denotes peptides of 36–43 amino acids that are crucially involved in Alzheimer's disease as the main component of the amyloid plaques found in the brains of Alzheimer patients. The peptides result from the amyloid precursor protein (APP), which is being cut by certain enzymes to yield Aβ. Aβ molecules can aggregate to form flexible soluble oligomers which may exist in several forms. It is now believed that certain misfolded oligomers (known as "seeds") can induce other Aβ molecules to also take the misfolded oligomeric form, leading to a chain reaction akin to a prion infection. The seeds or the resulting amyloid plaques are toxic to nerve cells. The other protein implicated in Alzheimer's disease, tau protein, also forms such prion-like misfolded oligomers, and there is some evidence that misfolded Aβ can induce tau to misfold.
A recent study suggested that APP and its amyloid potential is of ancient origins, dating as far back as early deuterostomes.
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