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Arch Neurol. 2001;58:351-352.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

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. . . . [Full Text of this Article]

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