ArticleActa neuropathologica communications2025
PPAR-γ activation by pioglitazone inhibits microglia-mediated neuroinflammation and alleviates disease in neuromyelitis optica spectrum disorders.
Article in Acta neuropathologica communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Microglia contribute to antibody-dependent cell-mediated cytotoxicity (ADCC) in neuromyelitis optica spectrum disorders (NMOSD). This complement-independent process has been implicated in early neuroinflammation following aquaporin-4 immunoglobulin G autoantibodies (AQP4-IgG) binding to astrocytes. We investigated whether pioglitazone, a clinically approved peroxisome proliferator-activated receptor gamma (PPARγ) agonist, could be repurposed to reduce complement-independent neuroinflammation driven by activated microglia and ameliorate disease in mice receiving passive transfers of human AQP4-IgG. Pioglitazone treatment alleviated motor impairments and NMOSD-like pathologies, associating with reduced microglial activation and pro-inflammatory cytokine levels. Antagonizing PPARγ reversed the beneficial effects of pioglitazone, indicating that these effects were PPARγ-dependent. Microglial depletion attenuated AQP4-IgG-induced motor impairments and pathologies, supporting the detrimental role of microglial activation. Serum levels of soluble triggering receptor expressed on myeloid cells 2 (sTREM2), a microglial activation biomarker, were increased in both the mouse model and patients with NMOSD. Pioglitazone reduced sTREM2, which were correlated with attenuated AQP4-IgG-induced microglial activation, neuroinflammation, and pathologies in mice. Elevated sTREM2 levels were associated with cytokines and chemokines related to activated microglia in patients with NMOSD, suggesting the clinical benefits of pioglitazone. Our findings highlight the potential of repurposing PPAR-γ agonists for reducing microglia-mediated neuroinflammation in acute NMOSD attacks.
Indexed as
Identifiers
What OpenQuestion holds
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 OpenQuestion graph.