Evidence map›Paper›PMID 33299135›Full record

ArticleMolecular psychiatry2021

AIM2 inflammasome mediates hallmark neuropathological alterations and cognitive impairment in a mouse model of vascular dementia.

Luting Poh, David Y Fann, Peiyan Wong, Hong Meng Lim, Sok Lin Foo, Sung-Wook Kang, Vismitha Rajeev, Sharmelee Selvaraji, Vinaya Rajagopal Iyer, Nageiswari Parathy and 9 more

Abstract read
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In one paragraph

Article in Molecular psychiatry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed, 2 pooled it
7.7field-weighted citation impact, top 2% 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

87 citing papers in PubMed, 2 syntheses or guidelines pooled it, 157 citations in OpenAlex.

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  18. [Prediction of immunotherapy targets for chronic cerebral hypoperfusion by bioinformatics method].Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi · 2025
    Article
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27 more citing papers are in PubMed but not listed here.

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

19 authors at 4 institutions in 4 countries.

Luting PohDepartment of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.ORCID http://orcid.org/0000-0001-5198-1505
David Y FannDepartment of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore. bchfywd@nus.edu.sg.
Peiyan WongDepartment of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
Hong Meng LimDepartment of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
Sok Lin FooDepartment of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
Sung-Wook KangDepartment of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
Vismitha RajeevDepartment of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
Sharmelee SelvarajiDepartment of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
Vinaya Rajagopal IyerDepartment of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.ORCID http://orcid.org/0000-0003-0631-8987
Nageiswari ParathyDepartment of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
Mohammad Badruzzaman KhanDepartment of Neurology, Medical College of Georgia, Augusta University, Augusta, GA, USA.
David C HessDepartment of Neurology, Medical College of Georgia, Augusta University, Augusta, GA, USA.
Dong-Gyu JoSchool of Pharmacy, Sungkyunkwan University, Suwon, Republic of Korea.ORCID http://orcid.org/0000-0003-2271-1076
Grant R DrummondDepartment of Physiology, Anatomy and Microbiology, La Trobe University, Bundoora, VIC, Australia.
Christopher G SobeyDepartment of Physiology, Anatomy and Microbiology, La Trobe University, Bundoora, VIC, Australia.
Mitchell K P LaiDepartment of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
Christopher Li-Hsian ChenDepartment of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
Lina H K LimDepartment of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
Thiruma V ArumugamDepartment of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore. g.arumugam@latrobe.edu.au.ORCID http://orcid.org/0000-0002-3377-0939
National University of Singapore · SGAugusta University · USLa Trobe University · AUSungkyunkwan University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic cerebral hypoperfusion is associated with vascular dementia (VaD). Cerebral hypoperfusion may initiate complex molecular and cellular inflammatory pathways that contribute to long-term cognitive impairment and memory loss. Here we used a bilateral common carotid artery stenosis (BCAS) mouse model of VaD to investigate its effect on the innate immune response-particularly the inflammasome signaling pathway. Comprehensive analyses revealed that chronic cerebral hypoperfusion induces a complex temporal expression and activation of inflammasome components and their downstream products (IL-1β and IL-18) in different brain regions, and promotes activation of apoptotic and pyroptotic cell death pathways. Polarized glial-cell activation, white-matter lesion formation and hippocampal neuronal loss also occurred in a spatiotemporal manner. Moreover, in AIM2 knockout mice we observed attenuated inflammasome-mediated production of proinflammatory cytokines, apoptosis, and pyroptosis, as well as resistance to chronic microglial activation, myelin breakdown, hippocampal neuronal loss, and behavioral and cognitive deficits following BCAS. Hence, we have demonstrated that activation of the AIM2 inflammasome substantially contributes to the pathophysiology of chronic cerebral hypoperfusion-induced brain injury and may therefore represent a promising therapeutic target for attenuating cognitive impairment in VaD.

Indexed as

Cognitive DysfunctionDementia, VascularWhite MatterAnimalsDisease Models, AnimalDNA-Binding ProteinsInflammasomesMiceMice, Inbred C57BLAim2 protein, mouseDNA-Binding ProteinsInflammasomes

Identifiers

PMID33299135
OpenAlexW3112474963

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.