Correlative memory deficits, Aβ elevation, and amyloid plaques in transgenic mice

Karen Hsiao, Paul Chapman, Steven Nilsen, Chris Eckman, Yasuo Harigaya, Steven Younkin, Fusheng Yang, Greg Cole

Research output: Contribution to journalArticlepeer-review

3504 Scopus citations


Transgenic mice overexpressing the 695-amino acid isoform of human Alzheimer β-amyloid (Aβ) precursor protein containing a Lys670 → Asn, Met671 → Leu mutation had normal learning and memory in spatial reference and alternation tasks at 3 months of age but showed impairment by 9 to 10 months of age. A fivefold increase in Aβ(1-40) and a 14-fold increase in Aβ(1-42/43) accompanied the appearance of these behavioral deficits. Numerous Aβ plaques that stained with Congo red dye were present in cortical and limbic structures of mice with elevated amounts of Aβ. The correlative appearance of behavioral, biochemical, and pathological abnormalities reminiscent of Alzheimer's disease in these transgenic mice suggests new opportunities for exploring the pathophysiology and neurobiology of this disease.

Original languageEnglish (US)
Pages (from-to)99-102
Number of pages4
Issue number5284
StatePublished - 1996

ASJC Scopus subject areas

  • General


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