ArticleJournal of neuroinflammation2026
Neural impairments caused by energy storage material NCM811 via aberrated synaptic pruning: role of Th17 cells in microglia polarization.
Article in Journal of neuroinflammation, 2026. 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
6 authors.
Funding
Abstract
introductionWith the development of green energy technology, the Nickel (Ni)0.8Cobalt(Co)0.1Manganese(Mn)0.1(OH)₂ (NCM811) precursor has been used as a cathode material for lithium batteries due to its high energy density. However, this raises a concern about the risk of NCM811 exposure during raw material processing, battery production, and recycling.
objectivesThis study aimed to investigate the neurotoxic effects of NCM811 particle exposure and the underlying mechanism.
methodsC57BL/6J mice were intranasally exposed to NCM811 particles. Then, spatial memory ability was assessed using the Morris water maze. Metal accumulation and distribution in brain regions were analyzed by laser ablation inductively coupled plasma mass spectrometry (LA-ICP-MS), and histopathological changes were examined by histological staining. The proportion of peripheral T helper type 17 (Th17) cells was measured by flow cytometry, and the concentration of IL-17A in brain tissue was determined by ELISA. The effect of IL-17A on microglia was further verified in il17ra knockout mice. Furthermore, an agonist of the cAMP pathway was administered to examine its protective effects against NCM811 exposure.
resultsNCM811exposure resulted in spatial memory impairment in mice, accompanied by increased Mn²⁺ deposition in the hippocampus and microglial M1 polarization. NCM811 exposure also increased the proportion of Th17 cells in the periphery, accompanied by enhanced Th17 cell infiltration and elevated IL-17A levels in brain tissues. Mechanistically, IL-17A activated microglia via the IL-17RA, suppressed the cAMP-CREB pathway, and promoted M1 polarization, subsequently leading to aberrant synaptic pruning and neurotransmitter dysregulation. Administration of a cAMP agonist blocked microglial M1 polarization induced by NCM811. Il17ra knockout mice effectively resisted these neural effects.
conclusionOur findings elucidate a novel mechanism by which NCM811 induces neurotoxicity through Th17 cell-mediated microglial polarization, providing potential therapeutic targets for cognitive dysfunction associated with battery material exposure in the context of green energy and sustainable development.
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.