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Maria Grazia Spillantini, PhD; Michel Goedert, MD, PhD

JAMA. 2001;286:2324-2326.

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

Filamentous deposits made of the microtubule-associated protein tau are a defining characteristic of a number of neurodegenerative diseases, including Alzheimer disease, progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), and some frontotemporal dementias, such as Pick disease.¹ The identification of coding region and intronic (noncoding) mutations in the tau gene in familial frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17) has established that dysfunction of tau protein is sufficient to cause neurodegeneration and dementia.^2-4

In recent years, it has become clear that what tau is to FTDP-17, the protein -synuclein is to Parkinson disease (PD). Mutations in the -synuclein gene are a rare cause of familial forms of PD,^5-6 and -synuclein is the major component of the filamentous inclusions of PD, the so-called Lewy bodies and Lewy neurites.⁷ The Lewy body inclusions that characterize several other diseases are also composed of -synuclein, . . . [Full Text of this Article]

Author Affiliations: Centre for Brain Repair and Department of Neurology, University of Cambridge (Dr Spillantini), and Medical Research Council Laboratory of Molecular Biology (Dr Goedert), Cambridge, England.

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