Abstract
The discovery of mutations in the tau gene in frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17) (1, 2, 3, 4) has demonstrated that tau dysfunction can result in neurodegeneration and has allowed researchers to generate transgenic models of the human tauopathies (5) (see Table 1 for summary). Transgenic models permit studies on the mechanisms of formation of filamentous tau lesions in neurons and glia as well as their role in neurodegeneration. They also serve as models to develop treatments for tauopathies.
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