Comparative Proteomic Analysis of Brains of Naturally Aging Mice
Abstract
We used comparative proteomic techniques to identify aging-related brain proteins in normal mice from neonate to old age. By 2-dimensional electrophoresis (2-DE), matrix assisted laser desorption/ionization time-of-flight (MALDI-TOF) mass spectrometry (MS) and peptide mass fingerprint (PMF) analysis, 39 proteins were identified, among which 6 stayed unchanged since 3 months, 6 increased and 27 decreased in various manners during aging. They are mainly involved in processes usually with destructive changes during aging, such as metabolism, transport, signaling, stress response and apoptosis. The 27 proteins' decrease may be responsible for brain aging. In particular, decrease of proteasome alpha subunits 3/6, ubiquitin carboxyl-terminal esterase L3, valosin-containing protein and calreticulin may be responsible for the declination of protein quality control; glutamate dehydrogenase 1, isocitrate dehydrogenase 1 and ubiquinol cytochrome c reductase core protein 2 for the shortage of energy and reducing agent; ubiquitin-conjugating enzyme E2N and heterogeneous nuclear ribonucleoprotein A2/B1 for the increase of DNA damage and transcription detuning; calbindin 1 and amphiphysin for the disturbance of synaptic transport and ion signals. The six proteins' increase may be involved in anti-aging processes. In particular, transketolase, mitochondrial creatine kinase 1 and ribosomal protein L37 may help to enhance energy metabolism; triosephosphate isomerase 1 may help to resist oxidative stress. Moreover, most of these proteins were found for the first time to be involved in the natural senescence of brain, which would provide new clues about the mechanism of brain aging.
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A lack of CoQ10 has been related to several conditions, including aging and neurological disorders.
“A lack of CoQ10 has been related to several conditions, including aging and neurological disorders [83,84,85,86,87,88,89] (Table 1).”
From The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence (2022) · cites this paper as [89]
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- Authors
- Yang, S., Liu, T., Li, S., Zhang, X., Ding, Q., Que, H., Yan, X., Wei, K., & Liu, S.
- Affiliations
- Institute of Basic Medical Sciences of the Chinese Academy of Medical Sciences (CN)
- National Center of Biomedical Analysis (CN)
- Venue
- Neuroscience
- Publisher
- Elsevier BV
- Published
- 2008-06
- Volume
- 154
- Issue
- 3
- Pages
- 1107-1120
- ISSN
- 0306-4522 (ISSN-L)
- OpenAlex
- W1991734112
- Cited by
- 82
- References
- 52
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 3 · 2023: 2 · 2022: 2 · 2021: 6 · 2020: 4 · 2019: 4 · 2018: 2 · 2017: 6 · 2016: 6 · 2015: 3 · 2014: 5 · 2013: 9 · 2012: 7
- FWCI
- 2.04
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Physical Sciences › Chemistry › Spectroscopy › Advanced Proteomics Techniques and Applications
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Antioxidants, Aging, Portulaca oleracea
- Keywords
- brain aging, mouse brain, protein quality control, VCP, calreticulin, energy metabolism, oxidative stress, DNA damage, anti-aging protein, transketolase
- MeSH terms
- Aging, Animals, Animals, Newborn, Brain, Brain Chemistry, Image Processing, Computer-Assisted, Male, Nerve Tissue Proteins, Neuropeptides, Blotting, Western, Electrophoresis, Gel, Two-Dimensional, Databases, Factual, Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization, Proteomics, Mice
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