Evidence mapPaperPMID 41299782Full record

ReviewTranslational neurodegeneration2025

Immunosenescence in aging and neurodegenerative diseases: evidence, key hallmarks, and therapeutic implications.

Zhichun Chen, Zixu Mao, Weiting Tang, Yuxuan Shi, Jun Liu, Yong You

Abstract readReview
In one paragraph

Review in Translational neurodegeneration, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

12 citing papers in PubMed.

  1. Lecanemab treatment improves B cell subpopulation immune homeostasis in patients with Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Zhichun ChenDepartment of Neurology, The Second Affiliated Hospital of Hainan Medical University, Haikou, 570311, China.
Zixu MaoDepartments of Pharmacology and Chemical Biology and Neurology, Emory University School of Medicine, Atlanta, GA, 30322, USA.
Weiting TangDepartment of Neurology, The Second Affiliated Hospital of Hainan Medical University, Haikou, 570311, China.
Yuxuan ShiDepartment of Neurology, The Second Affiliated Hospital of Hainan Medical University, Haikou, 570311, China.
Jun LiuDepartment of Neurology and Institute of Neurology, Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China. jly0520@hotmail.com.ORCID http://orcid.org/0000-0001-8300-8646
Yong YouDepartment of Neurology, The Second Affiliated Hospital of Hainan Medical University, Haikou, 570311, China. hy213440@muhn.edu.cn.

Funding

Hainan Provincial Natural Science Foundation of China 825MS173National Natural Science Foundation of China 81873778National Natural Science Foundation of China 82060213National Natural Science Foundation of China 82071415National Research Center for Translational Medicine at Shanghai, Ruijin NRCTM(SH)-2021-03Scientific Research Project of Hainan Higher Education Institutions Hnky2025-21
6 · The paper itself

Abstract

Aging is a multifaceted biological process affecting various organ systems. Immunosenescence, a key feature of aging, markedly increases susceptibility to infections, cancers, autoimmune diseases, and also neurodegenerative disorders. Immunosenescence not only accelerates normal aging but also drives the progression of neurodegenerative diseases, including Alzheimer's disease (AD) and Parkinson's disease (PD). However, the lack of a consensus on the mechanistic hallmarks of immunosenescence presents a major barrier to the development and validation of anti-aging therapies. In this review, we propose 11 hallmarks of immunosenescence: genomic instability, telomere attrition, epigenetic dysregulation, stem cell exhaustion, loss of proteostasis, deregulated nutrient-sensing, mitochondrial dysfunction, cellular senescence, chronic inflammation, altered intercellular communication, and microbiome dysbiosis. We also elucidate the intricate interplay between immunosenescence and both normal brain aging and neurodegenerative pathologies, highlighting the pivotal involvement of age-related immune dysregulation in the pathogenesis of neurodegenerative disorders. This mechanistic connection is particularly evident in prototypical neurodegenerative conditions such as AD and PD, where immunosenescence appears to significantly contribute to disease progression and phenotypic manifestations. Given that the ultimate goal of immune aging research is to prevent or alleviate age-related diseases, we also discuss potential hallmark-targeting anti-immunosenescence strategies to delay or even reverse normal aging and neurodegeneration.

Indexed as

AgingImmunosenescenceNeurodegenerative DiseasesAnimalsCellular SenescenceHumansAnti-aging therapyBrain agingHallmarksImmunosenescenceNeurodegenerative disease

Identifiers

PMID41299782
PMCPMC12659517

What Socratic holds

Textmetadata
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Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.