Genetic linkage studies in Alzheimer's disease families

M. A. Pericak-Vance, L. H. Yamaoka, C. S. Haynes, M. C. Speer, J. L. Haines, P. C. Gaskell, W. Y. Hung, C. M. Clark, A. L. Heyman, J. A. Trofatter, J. P. Eisenmenger, J. R. Gilbert, J. E. Lee, M. J. Alberts, D. V. Dawson, R. J. Bartlett, N. L. Earl, T. Siddique, J. M. Vance, P. M. ConneallA. D. Roses*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

118 Scopus citations


Alzheimer's disease is a devastating neurological disorder and the leading cause of dementia among the elderly. Recent studies have localized the gene for familial Alzheimer's disease to chromosome 21 in a series of early onset AD families (mean age of onset < 60). Familial late onset AD (mean age of onset > 60) is a more common clinical form of the disorder. Thirteen families with multiply affected Alzheimer's disease family members were identified and sampled. Ten of these families were of the late onset Alzheimer's disease type. Simulation studies were used to evaluate the usefulness of these pedigrees in linkage studies in familial Alzheimer's disease. Linkage studies undertaken to test the localization of both early onset and late onset Alzheimer's disease families to chromosome 21 failed to establish linkage and excluded linkage from a large portion of the region where the early onset Alzheimer's disease gene was localized. These findings suggest that more than one etiology may exist for familial Alzheimer's disease and indicate the need for continued screening of the genome in familial Alzheimer's disease families.

Original languageEnglish (US)
Pages (from-to)271-279
Number of pages9
JournalExperimental Neurology
Issue number3
StatePublished - Dec 1988

ASJC Scopus subject areas

  • Neurology
  • Developmental Neuroscience


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