Evidence map›Paper›PMID 34437570›Full record

ArticlePloS one2021

Three month inhalation exposure to low-level PM2.5 induced brain toxicity in an Alzheimer's disease mouse model.

Sheng-Han Lee, Yi-Hsuan Chen, Chu-Chun Chien, Yuan-Horng Yan, Hsin-Chang Chen, Hsiao-Chi Chuang, Hui-I Hsieh, Kuan-Hung Cho, Li-Wei Kuo, Charles C-K Chou and 4 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.9field-weighted citation impact, top 6% of its field
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

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.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 52 citations in OpenAlex.

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  6. Estimating the Effects of Hypothetical AmbientEnvironmental health perspectives · 2025
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4 · The record

Corrections and comments

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

14 authors at 9 institutions in 2 countries.

Sheng-Han LeeInstitute of Environmental and Occupational Health Sciences, College of Public Health, National Taiwan University, Taipei, Taiwan.
Yi-Hsuan ChenInstitute of Environmental and Occupational Health Sciences, College of Public Health, National Taiwan University, Taipei, Taiwan.
Chu-Chun ChienDepartment of Pathology, Kaohsiung Municipal Ta-Tung Hospital, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan.
Yuan-Horng YanDepartment of Endocrinology and Metabolism, Kuang Tien General Hospital, Taichung, Taiwan.ORCID 0000-0003-3865-9057
Hsin-Chang ChenInstitute of Food Safety and Health, College of Public Health, National Taiwan University, Taipei, Taiwan.
Hsiao-Chi ChuangSchool of Respiratory Therapy, College of Medicine, Taipei Medical University, Taipei, Taiwan.
Hui-I HsiehDepartment of Occupational Medicine, Cathay General Hospital, Taipei, Taiwan.
Kuan-Hung ChoInstitute of Biomedical Engineering and Nanomedicine, National Health Research Institutes, Miaoli, Taiwan.
Li-Wei KuoInstitute of Biomedical Engineering and Nanomedicine, National Health Research Institutes, Miaoli, Taiwan.
Charles C-K ChouResearch Center for Environmental Changes, Academia Sinica, Taipei, Taiwan.
Ming-Jang ChiuDepartment of Neurology, National Taiwan University Hospital, Taipei, Taiwan.
Boon Lead TeeDepartment of Neurology, Memory and Aging Center, University of California at San Francisco, San Francisco, California, United States of America.
Ta-Fu ChenDepartment of Neurology, National Taiwan University Hospital, Taipei, Taiwan.
Tsun-Jen ChengInstitute of Environmental and Occupational Health Sciences, College of Public Health, National Taiwan University, Taipei, Taiwan.ORCID 0000-0002-2613-8230
National Taiwan University · TWNational Health Research Institutes · TWNational Taiwan University Hospital · TWCathay General Hospital · TWKaohsiung Medical University Chung-Ho Memorial Hospital · TWKuang Tien General Hospital · TWResearch Center for Environmental Changes, Academia Sinica · TWTaipei Medical University · TWUniversity Memory and Aging Center · US

Funding

TDP-43 Loss-of-Function: Biology to BiomarkersP01AG019724 · NIA · UNIVERSITY OF PENNSYLVANIA · PI Jennifer Merrilees · 2002 to 2026
$67.2M
Chinese Language Assessment in Primary Progressive AphasiaR21AG068757 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI GORNO TEMPINI, MARIA LUISA · 2021 to 2022
$360k
NIA NIH HHS P01 AG019724NIA NIH HHS R21 AG068757
6 · The paper itself

Abstract

Although numerous epidemiological studies revealed an association between ambient fine particulate matter (PM2.5) exposure and Alzheimer's disease (AD), the PM2.5-induced neuron toxicity and associated mechanisms were not fully elucidated. The present study assessed brain toxicity in 6-month-old female triple-transgenic AD (3xTg-AD) mice following subchronic exposure to PM2.5 via an inhalation system. The treated mice were whole-bodily and continuously exposed to real-world PM2.5 for 3 months, while the control mice inhaled filtered air. Changes in cognitive and motor functions were evaluated using the Morris Water Maze and rotarod tests. Magnetic resonance imaging analysis was used to record gross brain volume alterations, and tissue staining with hematoxylin and eosin, Nissl, and immunohistochemistry methods were used to monitor pathological changes in microstructures after PM2.5 exposure. The levels of AD-related hallmarks and the oxidative stress biomarker malondialdehyde (MDA) were assessed using Western blot analysis and liquid chromatography-mass spectrometry, respectively. Our results showed that subchronic exposure to environmental levels of PM2.5 induced obvious neuronal loss in the cortex of exposed mice, but without significant impairment of cognitive and motor function. Increased levels of phosphorylated-tau and MDA were also observed in olfactory bulb or hippocampus after PM2.5 exposure, but no amyloid pathology was detected, as reported in previous studies. These results revealed that a relatively lower level of PM2.5 subchronic exposure from the environmental atmosphere still induced certain neurodegenerative changes in the brains of AD mice, especially in the olfactory bulb, entorhinal cortex and hippocampus, which is consistent with the nasal entry and spreading route for PM exposure. Systemic factors may also contribute to the neuronal toxicity. The effects of PM2.5 after a more prolonged exposure period are needed to establish a more comprehensive picture of the PM2.5-mediated development of AD.

Indexed as

Air PollutantsAlzheimer DiseaseAmyloid beta-PeptidesAnimalsBrainChromatography, LiquidCognitionDisease Models, AnimalHippocampusInhalation ExposureMagnetic Resonance ImagingMalondialdehydeMass SpectrometryMiceMice, TransgenicNeuronsAir PollutantsAmyloid beta-PeptidesMalondialdehydeParticulate Mattertau Proteins

Identifiers

PMID34437570
PMCPMC8389369
OpenAlexW3195199709

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

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.