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Chronically active: activation of microglial proteolysis in ageing and neurodegeneration

journal contribution
posted on 2015-03-05, 15:06 authored by Alexandra StolzingAlexandra Stolzing, Sebastian Sethe, Tilman Grune
One of the microglial cell functions is the removal of modified extracellular proteins in the brain. The connection between protein oxidation, proteolysis, and microglial activation is the topic of this review. The effect of various activation agents on microglial cells with regard to changes in substrate uptake, proteolytic capacity and degradation efficiency of different types of oxidized protein materials is reviewed. It is shown that different activation stimuli initiate substrate-specific modulation for uptake and proteolysis, influencing an array of factors including receptor expression, lysosomal pH, and proteasome subunit composition. Age-related alterations in activation and proteolytic capacity in microglial cells are also discussed. In ageing, proteolytic effectiveness is diminished, while microglial cells are chronically activated and lose the oxidative burst ability, possibly supporting a 'vicious circle' of macrophage-induced neurodegeneration. © W. S. Maney & Son Ltd.

Funding

TG was supported by the DFG, GRK1033 and SFB575.

History

School

  • Mechanical, Electrical and Manufacturing Engineering

Published in

Redox Report

Volume

10

Issue

4

Pages

207 - 213

Citation

STOLZING, A., SETHE, S. and GRUNE, T., 2005. Chronically active: activation of microglial proteolysis in ageing and neurodegeneration. Redox Report, 10 (4), pp. 207 - 213.

Publisher

© W. S. Maney & Son Ltd.

Version

  • VoR (Version of Record)

Publisher statement

This work is made available according to the conditions of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) licence. Full details of this licence are available at: https://creativecommons.org/licenses/by-nc-nd/4.0/

Publication date

2005

Notes

This article is closed access.

ISSN

1351-0002

eISSN

1351-0002

Language

  • en

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