Cited by 260Neuroinflammation and Neurodegeneration MechanismsTryptophan and brain disordersGenetics, Aging, and Longevity in Model Organisms

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Immune aging, dysmetabolism, and inflammation in neurological diseases

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Deleidi, Michela, JÃ¤ggle, Madeline, Rubino, Graziella·2015·Frontiers in Neuroscience

DOI 10.3389/fnins.2015.00172PMC PMC4453474

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Abstract

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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Figure 1 Immune aging, dysmetabolism, and inflammation in neurological diseases . The aging of the immune system is accompanied by a progressive senescence of immune cells (immunosenescence) and a chronic proinflammatory environment characterized by increased levels of cytokines and adipokines (inflammaging). These immune molecules modulate neuronal function and prime microglial cells and vulnerable neuronal populations. With aging, microglial cells also become senescent, lose their neuroprotective function and become more prone to abnormal inflammatory activation. Amyloid deposition and pathogenetic forms of α-synuclein activate microglia with the subsequent release of proinflammatory mediators. Aged dysfunctional mitochondria play a fundamental role in immunosenescence and age-related inflammation by the production of ROS and DAMPs that activate the NLRP3 inflammasome and immune cells triggering inflammatory reactions. In turn, inflammatory mediators aggravate mitochondrial dysfunction. High immune risk profile, infections and metabolic syndrome promote abnormal inflammatory reactions that contribute to disease onset and progression.CC BY · PubMed Central

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Authors: Deleidi, M., JÃ¤ggle, 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)
DOI: 10.3389/fnins.2015.00172
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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