@article{ref1,
title="Is there a genetic basis for the deposition of beta-amyloid after fatal head injury?",
journal="Cellular and molecular neurobiology",
year="1999",
author="Graham, D. I. and Gentleman, S. M. and Nicoll, J. A. and Royston, M. C. and McKenzie, J. E. and Roberts, G. W. and Mrak, R. E. and Griffin, W. S.",
volume="19",
number="1",
pages="19-30",
abstract="1. Alzheimer's disease is a heterogeneous disorder that may be caused by genetic or environmental factors or by a combination of both. Abnormalities in chromosomes 1, 14, and 21 have all been implicated in the pathogenesis of the early-onset form of the disease, while the epsilon 4 allele of the apolipoprotein E gene (on chromosome 19) is now recognized as a risk factor for early- and late-onset sporadic and familial Alzheimer's disease. 2. The best-established environmental trigger for the disease is a head injury, 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 is 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 providing the first evidence for a link between a genetic susceptibility (apoE epsilon 4) and an environmental trigger (head injury) in the development of Alzheimer-type pathology.<p /><p>Language: en</p>",
language="en",
issn="0272-4340",
doi="",
url="http://dx.doi.org/"
}