Immune aging, dysmetabolism, and inflammation in neurological diseases
Open accessAbstract
As we age, the immune system undergoes a process of senescence accompanied by the increased production of proinflammatory cytokines, a chronic subclinical condition named as "inflammaging". Emerging evidence from human and experimental models suggest that immune senescence also affects the central nervous system and promotes neuronal dysfunction, especially within susceptible neuronal populations. In this review we discuss the potential role of immune aging, inflammation and metabolic derangement in neurological diseases. The discovery of novel therapeutic strategies targeting age-linked inflammation may promote healthy brain aging and the treatment of neurodegenerative as well as neuropsychiatric disorders.
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Peripheral inflammaging leads to low-level production of inflammatory mediators in circulation (IL-6, TNF-α, CRP), which contribute to inflammatory environment in CNS.
“At the systemic level, peripheral inflammaging leads to low-level production of inflammatory mediators in the circulation, including IL-6, TNF-α, and C-reactive protein (CRP), which also contribute to the inflammatory environment in the CNS.36,49,116”
From Role of neuroinflammation in neurodegeneration development (2023) · cites this paper as [116]
The ‘Immunosenescence and inflammaging’ section describes low-grade inflammation with increased IL-6, TNF-α and acute-phase proteins; ‘Brain cell senescence and neuro-inflammaging’ says peripheral inflammaging can drive low-grade brain inflammation. The paper names CRP in its discussion of obesity-associated inflammation, but does not specifically identify it as a product of peripheral inflammaging or show that CRP itself contributes to CNS inflammation. The indexed passages provide section labels but no page numbers. (LLM, conf=0.84)
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- Authors
- Deleidi, M., Jäggle, M., & Rubino, G.
- Affiliations
- German Center for Neurodegenerative Diseases (DE)
- University of Tübingen (DE)
- Corresponding author
- Deleidi, Michela
- ORCID
- Deleidi, Michela
- Venue
- Frontiers in Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2015-06-03
- Volume
- 9
- Pages
- 172-172
- ISSN
- 1662-453X (ISSN-L)
- PMC
- PMC4453474
- OpenAlex
- W1486303545
- Cited by
- 260
- References
- 247
- Citations by year
- 2026: 15 · 2025: 12 · 2024: 18 · 2023: 27 · 2022: 37 · 2021: 23 · 2020: 26 · 2019: 26 · 2018: 28 · 2017: 26 · 2016: 17 · 2015: 5
- FWCI
- 2.02
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Frontiers in Neuroscience (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- DZNE Pub (submittedVersion, other-oa)
- Funders
- European Commission (304108)
- Fritz Thyssen Stiftung
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- immunosenescence, inflammaging, neuroinflammation, neurodegenerative diseases, neuropsychiatric disorders, inflammatory cytokines, brain aging, neuronal dysfunction, anti-inflammatory therapy
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