Final answer:
The beta amyloid peptides, implicated in Alzheimer's disease, are produced by the enzymatic cleavage of APP protein. Prion proteins normally prevent their aggregation, but mutant prion proteins can contribute to the formation of harmful plaques.
Step-by-step explanation:
The enzymes responsible for the production of beta amyloid peptides are part of the enzymatic cleavage of the APP protein (amyloid precursor protein). This process yields amyloid beta (Aβ) peptides that consist of 39-43 amino acids. Under normal conditions, these peptides are further digested to prevent accumulation. However, in the case of Alzheimer's disease, the formation of these peptides is unregulated, leading to the formation of beta amyloid plaques. Notably, prion proteins (PrPc) are believed to bind to Aβ peptides to prevent their aggregation into plaques. Nonetheless, when prion protein aggregation is induced by mutant PrP (PrPsc), it prevents prion proteins from binding to Aβ peptide, thereby contributing to the accumulation of Aβ and plaque formation.