Association of plasma clusterin concentration with severity, pathology, and progression in Alzheimer disease.

@article{Thambisetty2010AssociationOP,
  title={Association of plasma clusterin concentration with severity, pathology, and progression in Alzheimer disease.},
  author={Madhav Thambisetty and Andrew Simmons and Latha Velayudhan and A. S. M. Abdul Hye and James Campbell and Yi Zhang and Lars-Olof Wahlund and Eric Westman and Anna Kinsey and Andreas G{\"u}ntert and Petroula Proitsi and John G. Powell and Mirsada {\vC}au{\vs}evi{\'c} and R Killick and Katie Lunnon and Steven F Lynham and Martin Broadstock and Fahd Choudhry and David R. Howlett and Robert J. Williams and Sally Isabel Sharp and C. Mitchelmore and Catherine Tunnard and Rufina Leung and Catherine Foy and Darragh O'Brien and Gerome Breen and Simon J. Furney and Malcolm A. Ward and Iwona Kloszewska and Patrizia Mecocci and Hilkka Soininen and Magda Tsolaki and Bruno Vellas and Angela K. Hodges and Rena Lyons and Sue Parkins and J. Channing Richardson and Susan M. Resnick and Luigi Ferrucci and Dean F. Wong and Yun Zhou and Sebastian Muehlboeck and Alan Evans and Paul T Francis and Christian Spenger and Simon Lovestone},
  journal={Archives of general psychiatry},
  year={2010},
  volume={67 7},
  pages={739-48}
}
CONTEXT Blood-based analytes may be indicators of pathological processes in Alzheimer disease (AD). OBJECTIVE To identify plasma proteins associated with AD pathology using a combined proteomic and neuroimaging approach. DESIGN Discovery-phase proteomics to identify plasma proteins associated with correlates of AD pathology. Confirmation and validation using immunodetection in a replication set and an animal model. SETTING A multicenter European study (AddNeuroMed) and the Baltimore… CONTINUE READING
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Clusterin / apolipoprotein J was associated with atrophy of the entorhinal cortex , baseline disease severity , and rapid clinical progression in AD .
Clusterin / apolipoprotein J was associated with atrophy of the entorhinal cortex , baseline disease severity , and rapid clinical progression in AD .
These results demonstrate an important role of clusterin in the pathogenesis of AD and suggest that alterations in amyloid chaperone proteins may be a biologically relevant peripheral signature of AD .
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