ReviewFrontiers in immunology2026
Microglia heterogeneity and therapeutic strategies in Parkinson's disease.
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 3 papers.
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.
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
3 citing papers in PubMed.
- C-terminal Domain of the Heavy Chain of Tetanus Toxin Ameliorate Lipopolysaccharide Induced Hemiparkinsonism in Rats.Neurotoxicity research · 2026Article
- Acupuncture regulates neuroinflammation: microglial glucose metabolism reprogramming as a potential mediating mechanism.Frontiers in immunology · 2026Review
- Oligodendrocyte dysfunction in neurodegenerative diseases: pathological features, underlying mechanisms and therapeutic targeting.Frontiers in aging neuroscience · 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
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkinson's disease (PD) is the second most common neurodegenerative disorder, characterized by the progressive loss of dopaminergic neurons in the substantia nigra (SN) and the abnormal aggregation of α-synuclein (α-syn). PD exhibits features of a chronic inflammatory disease, significantly affecting peripheral organs and the central nervous system (CNS). Clinical signs include motor symptoms such as rigidity, bradykinesia, and tremor, as well as non-motor symptoms such as psychological and cognitive issues. Microglia are resident immune cells of the CNS, exhibiting high heterogeneity and playing a crucial role in the neuronal degeneration and inflammation associated with PD. In PD, microglia play dual roles: maintaining PD homeostasis by phagocytosing and clearing α-syn aggregates while simultaneously becoming dysfunctional due to aggregate overload. This dysfunction drives their transition to a pro-inflammatory phenotype, exacerbating neurotoxicity. Recently, technological advances like single-cell transcriptomics have revealed the diverse functions and changing phenotypic lineages of microglia in PD, providing new insights into their mechanisms. This review systematically describes the biological traits of microglia and their functional, spatial, genetic, and gender-related differences in PD neurodegeneration. It summarizes new intervention and treatment strategies targeting microglia, highlights recent progress and challenges in preclinical research and clinical trials, and offers guidance for developing precision therapies for PD focused on modulating microglial function.
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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.