The chaperone Clusterin in neurodegeneration-friend or foe?

Alzheimer's disease Clusterin extracellular chaperone neurodegeneration protein aggregation tau tauopathies

Journal

BioEssays : news and reviews in molecular, cellular and developmental biology
ISSN: 1521-1878
Titre abrégé: Bioessays
Pays: United States
ID NLM: 8510851

Informations de publication

Date de publication:
07 2022
Historique:
revised: 15 04 2022
received: 13 12 2021
accepted: 20 04 2022
pubmed: 7 5 2022
medline: 28 6 2022
entrez: 6 5 2022
Statut: ppublish

Résumé

Fibrillar protein aggregates are the pathological hallmark of a group of age-dependent neurodegenerative conditions, including Alzheimer's and Parkinson's disease. Aggregates of the microtubule-associated protein Tau are observed in Alzheimer's disease and primary tauopathies. Tau pathology propagates from cell to cell in a prion-like process that is likely subject to modulation by extracellular chaperones such as Clusterin. We recently reported that Clusterin delayed Tau fibril formation but enhanced the activity of Tau oligomers to seed aggregation of endogenous Tau in a cellular model. In contrast, Clusterin inhibited the propagation of α-Synuclein aggregates associated with Parkinson's disease. These findings raise the possibility of a mechanistic link between Clusterin upregulation observed in Alzheimer's disease and the progression of Tau pathology. Here we review the diverse functions of Clusterin in the pathogenesis of neurodegenerative diseases, focusing on evidence that Clusterin may act either as a suppressor or enhancer of pathology.

Identifiants

pubmed: 35521968
doi: 10.1002/bies.202100287
doi:

Substances chimiques

Clusterin 0

Types de publication

Journal Article Review Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

e2100287

Informations de copyright

© 2022 The Authors. BioEssays published by Wiley Periodicals LLC.

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Auteurs

Patricia Yuste-Checa (P)

Department of Cellular Biochemistry, Max Planck Institute of Biochemistry, Martinsried, Germany.
Munich Cluster for Systems Neurology (SyNergy), Munich, Germany.
Aligning Science Across Parkinson's (ASAP) Collaborative Research Network, Chevy Chase, Maryland, USA.

Andreas Bracher (A)

Department of Cellular Biochemistry, Max Planck Institute of Biochemistry, Martinsried, Germany.

F Ulrich Hartl (FU)

Department of Cellular Biochemistry, Max Planck Institute of Biochemistry, Martinsried, Germany.
Munich Cluster for Systems Neurology (SyNergy), Munich, Germany.
Aligning Science Across Parkinson's (ASAP) Collaborative Research Network, Chevy Chase, Maryland, USA.

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