Evidence map›Paper›PMID 37165444›Full record

ArticleJournal of neuroinflammation2023

The involvement of NLRP3 inflammasome in CUMS-induced AD-like pathological changes and related cognitive decline in mice.

Jia-Mei Li, Ting Hu, Xiao-Na Zhou, Ting Zhang, Jia-Hui Guo, Min-Yuan Wang, Yi-Lin Wu, Wen-Jun Su, Chun-Lei Jiang

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

Article in Journal of neuroinflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 2 pooled it
8.9field-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

36 citing papers in PubMed, 2 syntheses or guidelines pooled it, 58 citations in OpenAlex.

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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

9 authors at 1 institution in 1 country.

Jia-Mei Li *Department of Stress Medicine, Faculty of Psychology, Naval Medical University, Xiangyin Road 800, Shanghai, 200433, China.
Ting Hu *Department of Stress Medicine, Faculty of Psychology, Naval Medical University, Xiangyin Road 800, Shanghai, 200433, China.
Xiao-Na Zhou *Department of Stress Medicine, Faculty of Psychology, Naval Medical University, Xiangyin Road 800, Shanghai, 200433, China.
Ting ZhangDepartment of Stress Medicine, Faculty of Psychology, Naval Medical University, Xiangyin Road 800, Shanghai, 200433, China.
Jia-Hui GuoDepartment of Stress Medicine, Faculty of Psychology, Naval Medical University, Xiangyin Road 800, Shanghai, 200433, China.
Min-Yuan WangDepartment of Stress Medicine, Faculty of Psychology, Naval Medical University, Xiangyin Road 800, Shanghai, 200433, China.
Yi-Lin WuDepartment of Stress Medicine, Faculty of Psychology, Naval Medical University, Xiangyin Road 800, Shanghai, 200433, China.
Wen-Jun SuDepartment of Stress Medicine, Faculty of Psychology, Naval Medical University, Xiangyin Road 800, Shanghai, 200433, China. suwenjun1992@163.com.
Chun-Lei JiangDepartment of Stress Medicine, Faculty of Psychology, Naval Medical University, Xiangyin Road 800, Shanghai, 200433, China. cljiang@vip.163.com.
Second Military Medical University · CN

Funding

National Natural Science Foundation of China 32170931National Natural Science Foundation of China 82101607
6 · The paper itself

Abstract

backgroundNumerous studies have found that inhibiting the expression of NLRP3 inflammasome can significantly improve depressive-like behaviors in mice, but the research on its effect on cognitive decline in depression and its mechanism is still lacking. This study aimed to elucidate the role of NLRP3 inflammasome in cognitive decline in depression and explore the common neuro-immunological mechanisms of depression and Alzheimer's disease (AD).

methodsMale C57BL/6 mice were subjected to chronic unpredictable mild stress (CUMS) for 5 weeks, treatment group was administered with the NLRP3 inhibitor MCC950 (10 mg/kg, i.p.), fluoxetine served as positive control. Then, the mice were assessed for cognitive behaviors and depression-like behaviors, and changes of microglia and neurons in hippocampus and levels of Aβ metabolic pathway and tau protein were measured. To explore the mechanism of NLRP3 activation on neurons, we performed in vitro studies using BV2 microglia and mouse primary neurons. Furthermore, we focused on the role of NLRP3 inflammasome in the function of neurons and the expression of AD pathological indicators.

resultsCUMS induced depressive-like behaviors and cognitive decline in mice, which could be reversed by inhibiting NLRP3 inflammasome. MCC950, a specific NLRP3 inhibitor, alleviated CUMS-induced neuron injury and AD-like pathological changes, including the abnormal expression of Aβ metabolic pathway and the hyper-phosphorylation of tau protein. LPS (1 μg/mL) + ATP (1 mM) treatment activated the expression of NLRP3 inflammasome and IL-1β in vitro. In vitro experiment also proved that inhibiting the expression of NLRP3 inflammasome in microglia can restore the Aβ metabolic pathway to normal, decrease neuronal tau protein phosphorylation and protect neurons.

conclusionsInhibition of NLRP3 inflammasome effectively alleviated CUMS-induced depressive-like behaviors and cognitive decline in mice, and inhibited the activation of AD physiological indicators.

Indexed as

Alzheimer DiseaseCognitive DysfunctionAnimalsInflammasomesMaleMiceMice, Inbred C57BLNLR Family, Pyrin Domain-Containing 3 Proteintau ProteinsInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mousetau ProteinsAlzheimer’s diseaseCognitive declineDepressionNeuroinflammationNLRP3 inflammasome

Identifiers

PMID37165444
PMCPMC10173607
OpenAlexW4376131370

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.