作者: Lars Lannfelt , C. Nordstedt
DOI: 10.1007/978-3-7091-6781-6_17
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摘要: Considerable advances have been made the last years in understanding of pathogenesis Alzheimer’s disease (AD): Several pathogenic mutations found amyloid precursor protein gene on chromosome 21. Two other dominantly operating genes 14 and 1 were recently cloned, named presenilin 2, respectively. Mutations these give rise to AD with a very early age onset. Increased Aβ1-42 is most likely mechanism all cases. A susceptibility for has also found. There an association between ɛ4 allele apolipoprotein E (APOE) late-onset AD. The increases risk AD, although some homozygotes may live long life without developing by which APOE promotes development increased plaque formation. new knowledge mechanisms gives opportunities alternative strategies therapeutic intervention.