TY - JOUR PY - 1999// TI - Is there a genetic basis for the deposition of beta-amyloid after fatal head injury? JO - Cellular and molecular neurobiology A1 - Graham, D. I. A1 - Gentleman, S. M. A1 - Nicoll, J. A. A1 - Royston, M. C. A1 - McKenzie, J. E. A1 - Roberts, G. W. A1 - Mrak, R. E. A1 - Griffin, W. S. SP - 19 EP - 30 VL - 19 IS - 1 N2 - 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.
Language: en
LA - en SN - 0272-4340 UR - http://dx.doi.org/ ID - ref1 ER -