Beta-amyloid protein probe hybridized to chromosome 9 in 3 Alzheimer disease individuals.

E. C. Jenkins, E. A. Devine-Gage, X. L. Yao, G. E. Houck, W. T. Brown, N. K. Robakis, K. E. Wisniewski, W. P. Silverman, B. Reisberg, H. M. Wisniewski

Research output: Contribution to journalArticlepeer-review


We have reported recently the sublocalization of an Alzheimer Disease-associated gene that encodes for cerebrovascular beta-amyloid protein (BAP). Its locus appears to be at or proximal to band 21q2105 through band 21q11.1. We have also observed hybridization to chromosome 20 in normal and Down syndrome individuals using the single-stranded form of the probe. Further, we have found that BAP hybridizes to chromosome 9 in lymphoblastoid cells from three individuals from two families with familial Alzheimer Disease (AD). We have now obtained additional data which shows significant hybridization to chromosomes 9,20 and 21 for two normal control individuals, a Down syndrome (DS) individual and three AD individuals. When the normal and Down Syndrome individuals were compared to the group of individuals with AD, significant hybridization to chromosome 9 occurred in the Alzheimer group only (p less than .05). Almost half of the silver grains on chromosome 9 in the three AD individuals were localized to the distal area of the long arm. Whether these observations demonstrate an apparent genetic marker in these three individuals with familial AD, or whether our observations have identified a marker for both familial and sporadic AD will be determined by further studies.

Original languageEnglish (US)
Pages (from-to)269-275
Number of pages7
JournalProgress in clinical and biological research
StatePublished - 1989

ASJC Scopus subject areas

  • Medicine(all)


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