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Alzheimer's disease – do tauists and baptists finally shake hands?
The amyloid cascade hypothesis has been the predominant model of molecular pathogenesis in Alzheimer's disease. The finding of tau mutations in other dementias has added weight to the hypothesis as it suggests that tau-pathology is a downstream but essential part of the dementing process. Howev...
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Published in: | Trends in neurosciences (Regular ed.) 2002, Vol.25 (1), p.22-26 |
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Main Authors: | , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | The amyloid cascade hypothesis has been the predominant model of molecular pathogenesis in Alzheimer's disease. The finding of tau mutations in other dementias has added weight to the hypothesis as it suggests that tau-pathology is a downstream but essential part of the dementing process. However, some observations remain difficult to reconcile with the hypothesis. In transgenic mice, for example, amyloid generation does not induce the predicted cascade and in man, plaques and tangles are separated temporally and spatially. One alternative possibility is that some common factor, loss of
wnt signalling for example, might induce both plaques and tangles.
Is there a link between the tau hypothesis and the amyloid hypothesis of Alzheimer's disease? Are they both correct? The Wnt signalling pathway might hold the key. |
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ISSN: | 0166-2236 1878-108X |
DOI: | 10.1016/S0166-2236(00)02031-2 |