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Much of the current research effort in Parkinson disease (PD) focuses on finding common genetic variation that alters risk for, rather than causes, disease. While success has been relatively limited there are two genetic loci identified thus far that contain common variability robustly associated with risk for PD: the first is the gene SNCA, encoding α-synuclein,1 and the second is the genetic locus containing MAPT, the gene encoding microtubule-associated protein tau.
The association between MAPT and the tauopathies progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), and argyrophilic grain disease (AGD) is well-established. PSP, CBD, and AGD involve neurodegeneration with the deposition of tau in a range of neuronal and glial inclusions, including neurofibrillary tangles. On the face of it, an association between MAPT and PD, which involves alpha-synuclein deposition in Lewy bodies and Lewy neurites, but no tau deposition, seems less plausible. However, in this issue of Neurology®, Tobin and colleagues2 provide further evidence implicating …
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