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Learning and memory in the SAMP8 mouse

J F Flood1, J E Morley

  • 1Geriatric Research, Education and Clinical Center, St. Louis VA Medical Center, MO 63106, USA. jff31535@aol.com

Neuroscience and Biobehavioral Reviews
|March 10, 1998
PubMed
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The SAMP8 (P8) mouse model exhibits early-life learning and memory deficits, linked to amyloid beta and reduced NMDA receptor activity. These findings suggest P8 mice may model early Alzheimer-type dementia.

Area of Science:

  • Neuroscience
  • Aging Research
  • Animal Models

Background:

  • The SAMP8 (P8) mouse strain is characterized by premature aging, including cognitive decline.
  • Age-related deficits in learning and memory manifest early in P8 mice, impacting both aversive and appetitive tasks.

Purpose of the Study:

  • To review age-related changes in P8 mice.
  • To explore the utility of P8 mice as a model for early-stage Alzheimer-type dementia.

Main Methods:

  • Behavioral assessments of learning and memory acquisition and retention.
  • Anatomical, biochemical, and pharmacological analyses of the central nervous system.
  • Investigating the effects of amyloid beta antibodies and drug treatments on cognitive function.

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Main Results:

  • P8 mice show impaired learning and memory by 4 months of age.
  • Increased amyloid beta protein correlates with cognitive decline; antibody treatment shows therapeutic potential.
  • Reduced NMDA receptor activity is linked to memory impairment.
  • Pharmacological studies indicate impaired septohippocampal interactions contribute to memory deficits.

Conclusions:

  • P8 mice display significant age-related cognitive impairments.
  • Amyloid beta accumulation and reduced NMDA receptor activity are key factors.
  • P8 mice show promise as a model for studying early Alzheimer's disease