ArticleMolecular neurodegeneration advances2025
Adoptive NK cell transfer confers neuroprotection by attenuating neuroinflammation and alpha-synuclein pathology in a mouse model of synucleinopathy.
Article in Molecular neurodegeneration advances, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
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
Background: Natural killer (NK) cells are key effector lymphoid cells involved in both innate and adaptive immunity and are capable of clearing abnormally aggregated α-synuclein (αSyn). In preclinical Parkinson's disease (PD) models, NK cell depletion worsens motor deficits and increases insoluble αSyn accumulation, suggesting a neuroprotective role. However, the therapeutic potential of NK cell transfer in modulating αSyn pathology and neurodegeneration remains unexplored. Methods: To assess the efficacy of NK cell therapy, we administered biweekly systemic injections of untouched NK cells isolated from B6C3H donor mice into 2-month-old presymptomatic homozygous M83 transgenic mice injected with human αSyn preformed fibrils. Neurological function was assessed via clasping behavior and clinical scoring. αSyn pathology and dopaminergic neurodegeneration were evaluated via immunohistochemistry. CyTOF-based immune profiling and multiplex ELISA were performed to characterize central and peripheral immune responses. Results: Adoptive NK cell transfers improved motor function and reduced αSyn pathology in a region- and dose-dependent manner, with significant reductions in phosphorylated-αSyn inclusions and tyrosine hydroxylase-positive neuronal loss in the substantia nigra. NK cell transfer modulated the CNS immune landscape by reducing CD11b Conclusions: Our study provides direct evidence of NK cells exerting neuroprotective and immunomodulatory effects in a preclinical model of synucleinopathy. These findings support NK cell transfer as a novel therapeutic strategy for PD and related neurodegenerative disorders. Supplementary Information: The online version contains supplementary material available at 10.1186/s44477-025-00006-9.
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.