Molecular basis of memory loss in the TG2576 mouse model of Alzheimer's disease

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

Understanding the pathophysiology and treatment of Alzheimer's disease is vitally important. Alzheimer's disease threatens to affect currently at least 30% of all individuals currently alive in the 12 most financially developed countries, unless interventions are discovered to prevent or treat the disease. Although memory loss is the cardinal symptom of Alzheimer's disease, the pathophysiological mechanisms leading to cognitive deficits are poorly understood. It is difficult to address this problem in human studies, and impossible in cultured cells. Therefore, animal models are needed to elucidate the molecular mechanisms leading to dementia. A large number of animal models have focussed upon the role of amyloid plaques in the pathogenesis of Alzheimer's disease, because amyloid plaques are an essential diagnostic feature of the disease. However, the mechanism by which amyloid plaques or their principal molecular constituent, the amyloid-ß protein (Aß), disrupt cognitive function is not well understood. Herein, I describemy perspective on what we have learned about howAß impairs memory from research on Alzheimer's disease in mice and rats.

Original languageEnglish (US)
Pages (from-to)123-126
Number of pages4
JournalJournal of Alzheimer's Disease
Volume9
Issue numberSUPPL. 3
StatePublished - Jul 2006

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Memory Disorders
Alzheimer Disease
Amyloid Plaques
Animal Models
Serum Amyloid A Protein
Developed Countries
Cognition
Dementia
Cultured Cells
Research

Keywords

  • Aβ oligomers
  • Memory
  • Mice
  • Morris water maze
  • Operant behavioral task
  • Rats
  • Transgenic

Cite this

Molecular basis of memory loss in the TG2576 mouse model of Alzheimer's disease. / Ashe, Karen H.

In: Journal of Alzheimer's Disease, Vol. 9, No. SUPPL. 3, 07.2006, p. 123-126.

Research output: Contribution to journalArticle

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