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A Study of Familial Factors in Alzheimer's Disease

Published online by Cambridge University Press:  29 January 2018

L. J. Whalley
Affiliation:
M.R.C. Brain Metabolism Unit, Thomas Clouston Clinic, 152 Morningside Drive, Edinburgh, EH10 5LC, Scotland
A. D. Carothers
Affiliation:
M.R.C. Clinical and Population Cytogenetics Unit, Western General Hospital, Crewe Road, Edinburgh, EH4 2XU, Scotland
S. Collyer
Affiliation:
M.R.C. Clinical and Population Cytogenetics Unit, Western General Hospital, Crewe Road, Edinburgh, EH4 2XU, Scotland
R. De Mey
Affiliation:
M.R.C. Clinical and Population Cytogenetics Unit, Western General Hospital, Crewe Road, Edinburgh, EH4 2XU, Scotland
A. Frackiewicz
Affiliation:
M.R.C. Clinical and Population Cytogenetics Unit, Western General Hospital, Crewe Road, Edinburgh, EH4 2XU, Scotland

Summary

Data on the families of 74 probands with autopsy-proven Alzheimer's disease did not support the hypothesis, advanced by Heston and co-workers, of a familial association between Alzheimer's disease, Down's syndrome and immunoproliferative disorders. However, there are difficulties of interpreting negative conclusions in this type of study, particularly those resulting from small sample size and the impossibility of tracing all relatives; only the data for immunoproliferative disorders are incompatible with the hypothesis, those for Down's syndrome being too few to be informative. The incidence of presenile dementia among the first-degree relatives of probands was raised, as in many previous studies, and was consistent with a simple polygenic model. The mean parental age at birth of the probands was significantly raised by about 2 years (P = 0.01), but so also was that of their unaffected sibs, suggesting that the mechanism differs from that occurring in trisomy 21 and certain other aneuploidies.

Type
Research Article
Copyright
Copyright © Royal College of Psychiatrists, 1982 

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