The Role of Immunosenescence in Neurodegenerative Diseases
Open accessAbstract
Aging is characterized by the progressive decline of physiological function and tissue homeostasis leading to increased vulnerability, degeneration, and death. Aging-related changes of the innate and adaptive immune system include decline in the preservation and enhancement of many immune functions, such as changes in the number of circulating monocytic and dendritic cells, thymic involution, T cell polyfunctionality, or production of proinflammatory cytokines, and are defined as immunosenescence. Inflammatory functions are increased with age, causing the chronic low-grade inflammation, referred to as inflamm-aging, that contribute, together with immunosenescence, to neurodegenerative diseases. In this review, we discuss the link between the immune and nervous systems and how the immunosenescence and inflamm-aging can contribute to neurodegenerative diseases.
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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 [36]
Section 4 says systemic inflamm-aging can contribute to chronic low-grade inflammation in the CNS. Section 4.1 discusses circulating IL-6 and TNF-α and explains how peripheral cytokines may reach the brain. The cited paper does not identify CRP as one of these circulating mediators, so that part of the claim is unsupported. (LLM, conf=0.86)
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Plin2 Coordinates Immune and Metabolic Reprogramming in Lacrimal Gland Aging
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- Authors
- Costantini, E., D’Angelo, C., & Reale, M.
- Affiliations
- University of Chieti-Pescara (IT)
- Corresponding author
- Reale, Marcella
- Venue
- Mediators of Inflammation
- Publisher
- Wiley
- Published
- 2018
- Volume
- 2018
- Pages
- 1-12
- ISSN
- 0962-9351 (ISSN-L)
- 1466-1861
- PMC
- PMC5863336
- OpenAlex
- W2792949361
- Cited by
- 133
- References
- 126
- Citations by year
- 2026: 9 · 2025: 20 · 2024: 9 · 2023: 16 · 2022: 15 · 2021: 28 · 2020: 19 · 2019: 13 · 2018: 4
- FWCI
- 1.51
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Mediators of Inflammation (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)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Keywords
- immunosenescence, neurodegenerative diseases, inflammaging, aging, low-grade inflammation, innate immune system, adaptive immunity, thymic involution, T cell polyfunctionality, inflammatory cytokines, dendritic cells, monocytic cells, neuroinflammation
- MeSH terms
- Immunosenescence, Animals, Dendritic Cells, Humans, Immunity, Innate, Neurodegenerative Diseases
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