TAU, a microtubule-associated protein, facilitates the assembly and binding of microtubules. By supporting cytoskeletal structure and sustaining axonal transport, tau plays a fundamental role in the maintenance of neuronal survival.1 Long hypothesized as a protein with relevance to Alzheimer disease (AD), abnormally phosphorylated tau is a key component of the neurofibrillary tangle. In recent years the primary focus in AD has been on amyloid, not tau. This occurred in part because of the discovery that familial AD could be caused by mutations in the amyloid precursor protein. However, interest has shifted back toward tau with the finding that mutations in this protein are associated with a wide variety of degenerative disorders including frontotemporal dementia (FTD), progressive supranuclear palsy, corticobasal degeneration, and even AD. The article by Poorkaj and colleagues2 in this issue of the ARCHIVES fills an important gap in our understanding of the role of tau mutations in dementia. The continuing story relating tau to degenerative conditions represents one of the newest and most exciting developments in the entire field of dementia research.
Miller BL. Tau Mutations—Center Tent or Sideshow? Arch Neurol. 2001;58(3):351–352. doi:10.1001/archneur.58.3.351
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