Tau-mediated nuclear depletion and cytoplasmic accumulation of SFPQ in Alzheimer's and Pick's disease.

PloS One
Yazi D KeJürgen Götz

Abstract

Tau dysfunction characterizes neurodegenerative diseases such as Alzheimer's disease (AD) and frontotemporal lobar degeneration (FTLD). Here, we performed an unbiased SAGE (serial analysis of gene expression) of differentially expressed mRNAs in the amygdala of transgenic pR5 mice that express human tau carrying the P301L mutation previously identified in familial cases of FTLD. SAGE identified 29 deregulated transcripts including Sfpq that encodes a nuclear factor implicated in the splicing and regulation of gene expression. To assess the relevance for human disease we analyzed brains from AD, Pick's disease (PiD, a form of FTLD), and control cases. Strikingly, in AD and PiD, both dementias with a tau pathology, affected brain areas showed a virtually complete nuclear depletion of SFPQ in both neurons and astrocytes, along with cytoplasmic accumulation. Accordingly, neurons harboring either AD tangles or Pick bodies were also depleted of SFPQ. Immunoblot analysis of human entorhinal cortex samples revealed reduced SFPQ levels with advanced Braak stages suggesting that the SFPQ pathology may progress together with the tau pathology in AD. To determine a causal role for tau, we stably expressed both wild-type and P301L human tau...Continue Reading

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Citations

Sep 8, 2012·Cellular and Molecular Life Sciences : CMLS·Nicole Schonrock, Jürgen Götz
May 31, 2015·Neurobiology of Aging·Elyse Rosa, Margaret Fahnestock
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Nov 19, 2015·Frontiers in Aging Neuroscience·Illana Gozes, Yanina Ivashko-Pachima
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Jun 21, 2021·Acta Neuropathologica Communications·Harrison Tudor EvansJürgen Götz
Jul 16, 2021·BMJ Open Ophthalmology·Minwei WangJiantao Wang

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Methods Mentioned

BETA
transgenic
transfection
electrophoresis
PCR
confocal microscopy

Software Mentioned

SAGE

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