Work

Death or secretion? The demise of a plausible assumption about CSF-tau in Alzheimer Disease?

Year: 2012

Type: article

Abstract: Our recent identification of an exosomal route for tau protein secretion(1) marks a key similarity between tau and other aggregation-prone proteins implicated in neurodegenerative disease pathogenesis and is to some extent congruent with the popular idea that tau pathology spreads between neurons via a "prionlike" template-mediated protein misfolding mechanism in AD and other tauopathies. However, the observation that much of the phosphotau in CSF samples from early AD patients is exosomal (and thus likely to have been secreted) calls into question a very widely held and plausible assumption - the idea that the elevated CSF-tau in AD is due to the passive release and accumulation of tau in the CSF as a consequence of widespread neuronal death. Here we examine this issue directly and explore some of the broader implications of this study for our understanding of AD pathogenesis and the prospects for improving its diagnosis and treatment.

Source: Communicative & Integrative Biology

DOI: 10.4161/cib.21437

Authors: Garth F. Hall, Sudad Saman

Institution: University of Massachusetts Lowell

Language: English

Topic: Alzheimer's disease research and treatments

Subfield: Cellular and Molecular Neuroscience

Field: Neuroscience

Domain: Life Sciences

SDG: Good health and well-being

Open Access status: gold

Estimated APC paid: $1,459