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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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“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]
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Role of neuroinflammation in neurodegeneration development
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“BCSFB disruption impaired the selectivity of it, leading to increased infiltration of cytokines and leukocytes into the CSF which then activated glial cells in the CNS.144,145 BCSFB acts as a gateway for inflammationresolving leukocyte entry into the CSF during immune responses through the constitutively expressed adh…”
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The aging clock: circadian rhythms and later life
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Metadata
- 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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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