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β-Amyloid therapies in Alzheimer’s disease

2001; Taylor & Francis; Volume: 10; Issue: 4 Linguagem: Inglês

10.1517/13543784.10.4.593

1744-7658

Stanford S. Jhee, Thomas Shiovitz, Aaron W. Crawford, Neal R. Cutler,

Prion Diseases and Protein Misfolding

Neurones in the brain produce β-amyloid (Aβ) fragments from a larger precursor molecule termed the amyloid precursor protein (APP). When released from the cell, these protein fragments may accumulate in extracellular amyloid plaques and consequently hasten the onset and progression of Alzheimer's disease (AD). β-Amyloid fragments are generated through the action of specific proteases within the cell. Two of these enzymes, β- and γ-secretase, are particularly important in the formation of Aβ as they cleave within the APP protein to give rise to the N-terminal and C-terminal ends of the Aβ fragment, respectively. Consequently, many researchers are investigating therapeutic approaches that inhibit either β- or γ-secretase activity, with the ultimate goal of limiting Aβ production. An alternative AD therapeutic approach that is being investigated is to employ anti-Aβ antibodies to dissolve plaques that have already formed. Both of these approaches focus on the possibility that accrual of Aβ leads to neuronal degeneration and cognitive impairment characterised by AD and test the hypothesis that limiting Aβ deposition in neuritic plaques may be an effective treatment for AD.