Is there a genetic basis for the deposition of beta-amyloid after fatal head injury?

Citation
Di. Graham et al., Is there a genetic basis for the deposition of beta-amyloid after fatal head injury?, CELL MOL N, 19(1), 1999, pp. 19-30
Citations number
69
Categorie Soggetti
Neurosciences & Behavoir
Journal title
CELLULAR AND MOLECULAR NEUROBIOLOGY
ISSN journal
02724340 → ACNP
Volume
19
Issue
1
Year of publication
1999
Pages
19 - 30
Database
ISI
SICI code
0272-4340(199902)19:1<19:ITAGBF>2.0.ZU;2-5
Abstract
1. Alzheimer's disease is a heterogeneous disorder that may be caused by ge netic or environmental factors or by a combination of both. Abnormalities i n chromosomes 1, 14, and 21 have all been implicated in the pathogenesis of the early-onset form of the disease, while the epsilon 3 allele of the apo lipoprotein E gene (on chromosome 19) is nov: recognized as a risk factor f or early- and late-onset sporadic and familial Alzheimer's disease. 2. The best-established environmental trigger for the disease is a head inj ury, based on epidemiological and neuropathological evidence. Approximately 30% of patients who die after a single episode of severe head injury show intracerebral deposition of beta-amyloid protein (A beta), a protein that i s thought to be central to the pathogenesis of Alzheimer's disease. 3. Recent studies have revealed an over-representation of the apoE epsilon 4 allele in those head-injured patients displaying A beta pathology, thus p roviding the first evidence for a link between a genetic susceptibility (ap oE epsilon 4) and an environmental trigger (head injury) in the development of Alzheimer-type pathology.