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Small DH. The role of the amyloid protein precursor (APP) in Alzheimer's disease: does the normal function of APP explain the topography of neurodegeneration?. Neurochem Res. 1998;23(5):795-806doi: 10.1023/a:1022471729291.
Small, D. H. (1998). The role of the amyloid protein precursor (APP) in Alzheimer's disease: does the normal function of APP explain the topography of neurodegeneration?. Neurochemical research, 23(5), 795-806. https://doi.org/10.1023/a:1022471729291
Small, D H. "The role of the amyloid protein precursor (APP) in Alzheimer's disease: does the normal function of APP explain the topography of neurodegeneration?." Neurochemical research vol. 23,5 (1998): 795-806. doi: https://doi.org/10.1023/a:1022471729291
Small DH. The role of the amyloid protein precursor (APP) in Alzheimer's disease: does the normal function of APP explain the topography of neurodegeneration?. Neurochem Res. 1998 May;23(5):795-806. doi: 10.1023/a:1022471729291. PMID: 9566620.
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Neurochem Res. 1998 May;23(5):795-806. doi: 10.1023/a:1022471729291.

The role of the amyloid protein precursor (APP) in Alzheimer's disease: does the normal function of APP explain the topography of neurodegeneration?.

Neurochemical research

D H Small

Affiliations

  1. Department of Pathology, University of Melbourne, Parkville, Victoria, Australia. [email protected]

PMID: 9566620 DOI: 10.1023/a:1022471729291

Abstract

Alzheimer's disease (AD) is the most common form of dementia in the aged population. Early-onset familial AD (FAD) involves mutations in a gene on chromosome 21 encoding the amyloid protein precursor or on chromosomes 14 or 1 encoding genes known as presenilins. All mutations examined have been found to increase the production of amyloidogenic forms of the amyloid protein (A beta), a 4 kDa peptide derived from APP. Despite the remarkable progress in elucidating the biochemical mechanisms responsible for AD, little is known about the normal function of APP. A model of how APP and A beta are involved in pathogenesis is presented. This model may explain why certain neuronal populations are selectively vulnerable in AD. It is suggested that those neurons which more readily undergo neuritic sprouting and synaptic remodelling are more vulnerable to A beta neurotoxicity.

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