Final answer:
Beta amyloid (Aβ) is produced from the cleavage of amyloid precursor protein (APP) and is the main component of amyloid plaques in Alzheimer's disease. Normal degradation pathways prevent Aβ accumulation; however, in Alzheimer's, excess Aβ aggregates into plaques that are toxic to brain neurons.
Step-by-step explanation:
The relationship between beta amyloid (Aβ) and amyloid precursor protein (APP) is that Aβ is a peptide formed by the enzymatic cleavage of APP. Alzheimer's disease is characterized by the accumulation of beta amyloid plaques, which are primarily made up of Aβ peptide.
When APP is digested by enzymes, Aβ peptides, consisting of 39-43 amino acids, are produced. Under normal circumstances, these peptides are further degraded and do not accumulate. However, in Alzheimer's disease, these peptides misfold, become insoluble, and form aggregates known as amyloid plaques (as illustrated in the figures).
These plaques disrupt normal brain function and are a hallmark of the disease. Prion proteins (PrPc) can bind Aβ and prevent aggregation, but disturbances in prion protein function, such as in the case of mutant PrP (PrPsc), can promote the buildup of Aβ and plaque formation.