Plaques, tangles, and memory loss in mouse models of neurodegeneration.
Within the past decade, our understanding of the pathogenic mechanisms in Alzheimer's disease (AD) has dramatically advanced because of the development of transgenic mouse models that recapitulate the key pathological and behavioral phenotypes of the disease. These mouse models have allowed investigators to test detailed questions about how pathology develops and to evaluate potential therapeutic approaches that could slow down the development of this disease. In this review, we discuss the status of transgenic mouse models and review the complex relationship between pathology and behavior in the development of neuropathological syndromes in AD.
Eriksen
Jason L
JL
Department of Neuroscience, Mayo Clinic Jacksonville, 4500 San Pablo Road, Jacksonville, FL 32224, USA.
Janus
Christopher G
CG
D000544:Alzheimer Disease / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D016229:Amyloid beta-Peptides / Q000378:metabolism; D000818:Animals; D003072:Cognition Disorders / Q000378:metabolism; D004195:Disease Models, Animal; D006801:Humans; D008569:Memory Disorders / Q000235:genetics* / Q000473:pathology; D051379:Mice; D008822:Mice, Transgenic; D016874:Neurofibrillary Tangles / Q000378:metabolism* / Q000473:pathology; D058225:Plaque, Amyloid / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D016875:tau Proteins / Q000378:metabolism
D016229:Amyloid beta-Peptides; C054369:MAPT protein, human; D016875:tau Proteins