Cited by 133Neuroinflammation and Neurodegeneration MechanismsGenetics, Aging, and Longevity in Model OrganismsTryptophan and brain disorders

The Role of Immunosenescence in Neurodegenerative Diseases

Open access
Costantini, Erica, D’Angelo, Chiara, Reale, Marcella·2018·Mediators of Inflammation

Abstract

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.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1155/2018/6039171

Cites

126 of 126 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • 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)

    Experimental — accuracy not yet measured

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

Flagged first, then by citations

Cited by

Sorted by citations

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
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
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

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.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review