Editorials

Alzheimer's disease

BMJ 1994; 308 doi: https://doi.org/10.1136/bmj.308.6930.672 (Published 12 March 1994) Cite this as: BMJ 1994;308:672
  1. M Owen,
  2. M Liddell,
  3. P McGuffin

    Alzheimer's disease accounts for around half of all cases of senile dementia. Its prevalence increases steeply with age, from less than 1% at age 65 to 15% in the ninth decade.1 Until last year advances in understanding the genetics of the disease had been confined to a rare variant known as familial Alzheimer's disease, which is of unusually early onset and segregates in an autosomal dominant fashion. Between 15% and 20% of familial Alzheimer's disease is caused by mutations in the amyloid precursor protein gene on chromosome 212 - a small fragment of this protein, known as ß amyloid is one of the main constituents of senile plaques. A second gene, which probably accounts for most familial Alzheimer's disease, has been mapped to the long arm of chromosome 14 but has not yet been identified.3

    Familial Alzheimer's disease accounts for less than 1% of all cases of Alzheimer's disease. The genetics of the common variety are more complex. A large body of evidence indicates that this variety is familial, but unlike familial Alzheimer's disease it does not show a mendelian pattern of segregation, and less than half of all patients with the disease have a family history. Not surprisingly, the risk to relatives …

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