ReviewFrontiers in immunology2026
Immunosenescence and inflammaging in Parkinson's disease: mechanisms and therapeutic prospects.
Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
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.
Who cites it
2 citing papers in PubMed.
- Sex-Specific Systemic Signatures in Parkinson's Disease: Integrated Biochemical and Metabolomic Evidence.Biomedicines · 2026Article
- Artificial intelligence and machine learning in immunosenescence: from biomarker discovery to clinical translation.Frontiers in aging · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkinson's disease (PD) is characterized by the progressive loss of dopaminergic neurons, with growing evidence underscoring the critical role of immunosenescence-the age-related dysregulation of the immune system-in its pathogenesis. This review delineates the intricate interplay between systemic immunosenescence, chronic neuroinflammation, and neurodegeneration in PD. We explore how age-related remodeling of the peripheral immune system, termed "inflammaging," promotes a pro-inflammatory milieu that compromises blood-brain barrier integrity and drives microglial activation within the central nervous system. A central focus is the senescence-associated secretory phenotype, a cocktail of pro-inflammatory factors released by senescent glial cells, which perpetuates a self-sustaining cycle of neuroinflammation, facilitates the propagation of pathological α-synuclein, and ultimately accelerates neuronal loss. The review further examines the disruption of vital neuroimmune communication pathways, including aberrant neuron-glia and gut-brain axis signaling, which are corrupted in the aging brain. We evaluate the translational promise of emerging therapeutic strategies designed to target this immunosenescence-neuroinflammation axis. These include senolytic agents to clear senescent cells, adoptive regulatory T-cell therapy, cytokine-targeted immunomodulation, and immune rejuvenation approaches. Finally, we discuss significant translational challenges and outline future research directions, emphasizing the need for advanced model systems, biomarker development, and AI-driven personalized medicine to successfully develop disease-modifying immunotherapies that disrupt the vicious cycle of immunosenescence and neurodegeneration in PD.
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Registered trials
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.