Abstract
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 Aβ (amyloid β) and tau. This paper presents my perspective on what we have learnt about mechanisms of memory loss from Aβ and tau mouse models of Alzheimer's disease.
Original language | English (US) |
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Pages (from-to) | 591-594 |
Number of pages | 4 |
Journal | Biochemical Society transactions |
Volume | 33 |
Issue number | 4 |
DOIs | |
State | Published - Aug 2005 |
Keywords
- APP transgenic mice
- Alzheimer's disease
- Amyloid plaque
- Aβ
- Memory loss
- Tau