Regulation of Alzheimer β-amyloid precursor trafficking and metabolism11Portions of this review have previously appeared in Trends in Endocrinology and Metabolism and are reprinted here with the permission of Elsevier Publishing.
- Gandy, Sam
- Petanceska, Suzana
DOIAbstract
AbstractAlzheimer’s disease (AD) is characterized by the intracranial accumulation of the 4 kDa amyloid-β peptide (Aβ), following proteolysis of a ∼700-amino acid, integral membrane precursor, the Alzheimer amyloid precursor protein (APP). The best evidence causally linking APP to AD has been provided by the discovery of mutations within the APP coding sequence that segregate with disease phenotypes in autosomal dominant forms of familial AD (FAD). Though FAD is rare (<10% of all AD), the hallmark features (amyloid plaques, neurofibrillary tangles, synaptic and neuronal loss, neurotransmitter deficits and dementia) are indistinguishable when FAD is compared with typical, common, ‘non-familial’, or sporadic, AD (SAD). Studies of some clinica...
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