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The current understanding of the role of amyloid in Alzheimer's disease (AD) has been established by a remarkable congruence of multiple disciplines: neuropathology, biochemistry, molecular biology, and epidemiological genetics. It is known that amyloidβ is derived, by two sequential cleavages, from the receptor-like amyloid precursor protein (APP). The proteases involved are beta-secretase, identified as the novel aspartyl protease BACE, and gamma-secretase, a multimeric complex containing the presenilins (PS-1, PS-2). BACE1 and BACE2 have been isolated as homologue of BACE.
The current understanding of the role of amyloid in Alzheimer's disease (AD) has been established by a remarkable congruence of multiple disciplines: neuropathology, biochemistry, molecular biology, and epidemiological genetics. It is known that amyloidβ is derived, by two sequential cleavages, from the receptor-like amyloid precursor protein (APP). The proteases involved are beta-secretase, identified as the novel aspartyl protease BACE, and gamma-secretase, a multimeric complex containing the presenilins (PS-1, PS-2). BACE1 and BACE2 have been isolated as homologue of BACE.