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

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

Research output: Contribution to journalArticle

3327 Citations (Scopus)

Abstract

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
JournalScience
Volume274
Issue number5284
DOIs
StatePublished - 1996

Fingerprint

Serum Amyloid A Protein
Amyloid Plaques
Memory Disorders
Transgenic Mice
Congo Red
Neurobiology
Alzheimer Disease
Protein Isoforms
Coloring Agents
Learning
Amino Acids
Mutation
Spatial Memory

ASJC Scopus subject areas

  • General

Cite this

Hsiao, K., Chapman, P., Nilsen, S., Eckman, C., Harigaya, Y., Younkin, S. G., ... Cole, G. (1996). Correlative memory deficits, Aβ elevation, and amyloid plaques in transgenic mice. Science, 274(5284), 99-102. https://doi.org/10.1126/science.274.5284.99

Correlative memory deficits, Aβ elevation, and amyloid plaques in transgenic mice. / Hsiao, Karen; Chapman, Paul; Nilsen, Steven; Eckman, Chris; Harigaya, Yasuo; Younkin, Steven G; Yang, Fusheng; Cole, Greg.

In: Science, Vol. 274, No. 5284, 1996, p. 99-102.

Research output: Contribution to journalArticle

Hsiao, K, Chapman, P, Nilsen, S, Eckman, C, Harigaya, Y, Younkin, SG, Yang, F & Cole, G 1996, 'Correlative memory deficits, Aβ elevation, and amyloid plaques in transgenic mice', Science, vol. 274, no. 5284, pp. 99-102. https://doi.org/10.1126/science.274.5284.99
Hsiao, Karen ; Chapman, Paul ; Nilsen, Steven ; Eckman, Chris ; Harigaya, Yasuo ; Younkin, Steven G ; Yang, Fusheng ; Cole, Greg. / Correlative memory deficits, Aβ elevation, and amyloid plaques in transgenic mice. In: Science. 1996 ; Vol. 274, No. 5284. pp. 99-102.
@article{05152beae7824c69b0edcd486b4a480a,
title = "Correlative memory deficits, Aβ elevation, and amyloid plaques in transgenic mice",
abstract = "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.",
author = "Karen Hsiao and Paul Chapman and Steven Nilsen and Chris Eckman and Yasuo Harigaya and Younkin, {Steven G} and Fusheng Yang and Greg Cole",
year = "1996",
doi = "10.1126/science.274.5284.99",
language = "English (US)",
volume = "274",
pages = "99--102",
journal = "Science",
issn = "0036-8075",
publisher = "American Association for the Advancement of Science",
number = "5284",

}

TY - JOUR

T1 - Correlative memory deficits, Aβ elevation, and amyloid plaques in transgenic mice

AU - Hsiao, Karen

AU - Chapman, Paul

AU - Nilsen, Steven

AU - Eckman, Chris

AU - Harigaya, Yasuo

AU - Younkin, Steven G

AU - Yang, Fusheng

AU - Cole, Greg

PY - 1996

Y1 - 1996

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=0029742199&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0029742199&partnerID=8YFLogxK

U2 - 10.1126/science.274.5284.99

DO - 10.1126/science.274.5284.99

M3 - Article

VL - 274

SP - 99

EP - 102

JO - Science

JF - Science

SN - 0036-8075

IS - 5284

ER -