Mechanisms of memory loss in Abeta and tau mouse models.
Although memory loss is the central symptom of Alzheimer's disease, the pathophysiological mechanisms leading to dementia are poorly understood. It is difficult to answer this issue with studies in humans and impossible in cultured cells. Therefore animal models are needed to elucidate the molecular mechanisms leading to dementia. The chief neuropathological changes during Alzheimer's disease, namely neurofibrillary tangles and amyloid plaques, have helped us to determine which molecules to focus upon in the animal models, specifically Abeta (amyloid beta) and tau. This paper presents my perspective on what we have learnt about mechanisms of memory loss from Abeta and tau mouse models of Alzheimer's disease.
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Department of Neurology and Neuroscience, University of Minnesota, Minneapolis, MN 55455, USA. hsiao005@umn.edu
D000544:Alzheimer Disease / Q000235:genetics*; D016564:Amyloid beta-Protein Precursor / Q000235:genetics*; D000818:Animals; D004195:Disease Models, Animal; D006801:Humans; D008569:Memory Disorders / Q000235:genetics*; D051379:Mice; D008822:Mice, Transgenic; D016874:Neurofibrillary Tangles / Q000473:pathology; D015203:Reproducibility of Results; D016875:tau Proteins / Q000235:genetics*
D016564:Amyloid beta-Protein Precursor; D016875:tau Proteins