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• W2017355002 abstract "Alzheimer's disease (AD) is the major cause of dementia in the U.K. The clinical diagnosis of the specific disease resulting in dementia is unreliable and thus a definitive diagnosis of AD is best made in conjunction with post-mortem findings of amyloid plaques and neurofibrillary tangles. Alzheimer's disease is neuropathologically indistinguishable in the young and old, but has been divided arbitrarily into early- and late-onset disease using age cut-offs of 60 or 65 years. Twin and family studies suggest that genetic factors play a major role in its aetiology. This review considers the three loci which have been shown to be associated with early-onset AD: amyloid precursor protein, presenilin (PS)-l and PS-2. Mutations in these genes seem to be associated with overproduction of the 42-amino acid form of β-bamyloid, suggesting that this may be a central pathological process in AD. The impact of the different apo E alleles on the risks for late- and early-onset AD is discussed and compared with other dementing conditions. Recent analyses suggest that there are likely to be other genes besides apo E which impact on late-onset AD risk. The possible roles in AD of the mitochondria) mutation at position 4336, the PS intron 8 polymorphism, and variants in the alpha I-antichymotrypsin and VLDL-receptor genes, are considered." @default.
• W2017355002 created "2016-06-24" @default.
• W2017355002 creator A5008236816 @default.
• W2017355002 date "1997-08-01" @default.
• W2017355002 modified "2023-10-12" @default.
• W2017355002 title "The genetics of Alzheimer's disease" @default.
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• W2017355002 doi "https://doi.org/10.1016/s0301-0082(97)00014-2" @default.
• W2017355002 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/9316155" @default.
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