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  Aging in mouse brain is a cell/tissue-level phenomenon exacerbated by proteasome loss

Mao, L., Römer, I., Nebrich, G., Klein, O., Koppelstatter, A., Hin, S. C., et al. (2010). Aging in mouse brain is a cell/tissue-level phenomenon exacerbated by proteasome loss. Journal of Proteome Research, 9(7), 3551-3560. doi:10.1021/pr100059j.

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Item Permalink: https://hdl.handle.net/11858/00-001M-0000-0010-7AB4-A Version Permalink: https://hdl.handle.net/11858/00-001M-0000-0010-7AB5-8
Genre: Journal Article
Alternative Title : J Proteome Res

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 Creators:
Mao, L.1, Author
Römer, I.1, Author
Nebrich, G., Author
Klein, O.1, Author
Koppelstatter, A., Author
Hin, S. C., Author
Hartl, D.1, Author
Zabel, C.1, Author
Affiliations:
1Max Planck Society, ou_persistent13              

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Free keywords: aging; mouse brain; proteome; proteasome; redundancy; reliability theory
 Abstract: Biological aging is often described by its phenotypic effect on individuals. Still, its causes are more likely found on the molecular level. Biological organisms can be considered as reliability-engineered, robust systems and applying reliability theory to their basic nonaging components, proteins, could provide insight into the aging mechanism. Reliability theory suggests that aging is an obligatory trade-off in a fault-tolerant system such as the cell which is constructed based on redundancy design. Aging is the inevitable redundancy loss of functional system components, that is proteins, over time. In our study, we investigated mouse brain development, adulthood, and aging from embryonic day 10 to 100 weeks. We determined redundancy loss of different protein categories with age using reliability theory. We observed a near-linear decrease of protein redundancy during aging. Aging may therefore be a phenotypic manifestation of redundancy loss caused by nonfunctional protein accumulation. This is supported by a loss of proteasome system components faster than dictated by reliability theory. This loss is highly detrimental to biological self-renewal and seems to be a key contributor to aging and therefore could represent a major target for therapies for aging and age-related diseases.

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Language(s): eng - English
 Dates: 2010-07-02
 Publication Status: Issued
 Pages: -
 Publishing info: -
 Table of Contents: -
 Rev. Type: -
 Identifiers: eDoc: 539737
URI: http://www.ncbi.nlm.nih.gov/pubmed/20469937
DOI: 10.1021/pr100059j
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Title: Journal of Proteome Research
  Alternative Title : J Proteome Res
Source Genre: Journal
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Pages: - Volume / Issue: 9 (7) Sequence Number: - Start / End Page: 3551 - 3560 Identifier: ISSN: 1535-3893