Evidence map›Paper›PMID 41617938›Full record

ArticleNeurotoxicity research2026

Neurotoxicity Mechanisms of Per- and Polyfluoroalkyl Substances: An Integrated Study of Network Toxicology, Molecular Docking, and Mendelian Randomization.

Zhuoya Jiang, Chenchen Wei, Aijun Ma

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Article in Neurotoxicity research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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1citing papers in PubMed
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1 · What the graph read from it

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.

2 · The registry

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

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4 · The record

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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors.

Zhuoya JiangInstitute of Cerebrovascular Disease, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, 266000, China.
Chenchen WeiInstitute of Cerebrovascular Disease, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, 266000, China.
Aijun MaInstitute of Cerebrovascular Disease, The Affiliated Hospital of Qingdao University, Qingdao, Shandong, 266000, China. drmaj@qdu.edu.cn.

Funding

National Natural Science Foundation of China 82371331National Natural Science Foundation of China 82401545Natural Science Foundation of Shandong Province ZR2022QH363
6 · The paper itself

Abstract

backgroundObservational studies have shown that exposure to per- and polyfluoroalkyl substances can lead to neurotoxicity. We focus on whether perfluorooctanoic acid (PFOA) and perfluorooctane sulfonate (PFOS) affect brain morphology and the potential molecular mechanisms of toxicity.

methodsCausal relationship between exposure to both PFOA and PFOS and brain morphology was explored based on Mendelian randomization (MR), and the toxic molecular mechanism was investigated using network toxicology.

resultsMR analysis indicated PFOA exposure reduced brain volume in left parahippocampal (p = 0.018) and right rostral anterior cingulate (p = 0.007), while PFOS exposure decreased volume in left middle temporal (p = 0.036), paracentral (p = 0.022), postcentral (p = 0.014), posterior cingulate (p = 0.002), rostral middle frontal (p = 0.040), superior frontal (p = 0.027), superior parietal (p = 0.033), and in the right hemisphere: inferior parietal (p = 0.017), superior frontal (p = 0.030), superior parietal (p = 0.025), and caudal middle frontal (p = 0.041). GO/KEGG analyses revealed 161 targets linked to the neurotoxicity of PFOA and PFOS, primarily associated with fatty acid metabolism, GABA signaling, neurotransmitter receptor activity, ferroptosis, and PPAR pathways. Molecular docking verified key targets (PPARG, FASN, SCD, CD36, GOT2) underlying the toxicity mechanism.

conclusionsExposure to PFOA and PFOS leads to reduced brain volume - neurotoxicity at the macroscopic level. At the molecular level, we identified PPARG, FASN, SCD, CD36, and GOT2 as key targets implicated in the pathology of brain damage induced by PFOA and PFOS.

Indexed as

Alkanesulfonic AcidsBrainCaprylatesFluorocarbonsMolecular Docking SimulationNeurotoxicity SyndromesHumansMendelian Randomization AnalysisAlkanesulfonic AcidsCaprylatesFluorocarbonsperfluorooctane sulfonic acidperfluorooctanoic acidBrain morphometryNeurotoxicityPer- and polyfluoroalkyl substancesPerfluorooctanesulfonic acidPerfluorooctanoic acid

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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.