Evidence map›Paper›PMID 37177836›Full record

ArticleAging cell2023

Absent in melanoma 2 mediates aging-related cognitive dysfunction by acting on complement-dependent microglial phagocytosis.

Lei Ye, Shu Shu, Junqiu Jia, Min Sun, Siyi Xu, Xinyu Bao, Huijie Bian, Yi Liu, Meijuan Zhang, Xiaolei Zhu and 2 more

Open access · goldAbstract read
In one paragraph

Article in Aging cell, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

15 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Article
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  10. The Critical Role of Autophagy and Phagocytosis in the Aging Brain.International journal of molecular sciences · 2024
    Review
  11. Article
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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

12 authors at 2 institutions in 1 country.

Lei YeDepartment of Neurology, Nanjing Drum Tower Hospital, Medical School and The State Key Laboratory of Pharmaceutical Biotechnology, Institute of Translational Medicine for Brain Critical Diseases, Medical School, Nanjing University, Nanjing, China.
Shu ShuDepartment of Neurology, Nanjing Drum Tower Hospital, Medical School and The State Key Laboratory of Pharmaceutical Biotechnology, Institute of Translational Medicine for Brain Critical Diseases, Medical School, Nanjing University, Nanjing, China.
Junqiu JiaDepartment of Neurology, Nanjing Drum Tower Hospital, Medical School and The State Key Laboratory of Pharmaceutical Biotechnology, Institute of Translational Medicine for Brain Critical Diseases, Medical School, Nanjing University, Nanjing, China.
Min SunDepartment of Neurology, Nanjing Drum Tower Hospital, Medical School and The State Key Laboratory of Pharmaceutical Biotechnology, Institute of Translational Medicine for Brain Critical Diseases, Medical School, Nanjing University, Nanjing, China.
Siyi XuDepartment of Neurology, Nanjing Drum Tower Hospital, Medical School and The State Key Laboratory of Pharmaceutical Biotechnology, Institute of Translational Medicine for Brain Critical Diseases, Medical School, Nanjing University, Nanjing, China.
Xinyu BaoDepartment of Neurology, Nanjing Drum Tower Hospital, Medical School and The State Key Laboratory of Pharmaceutical Biotechnology, Institute of Translational Medicine for Brain Critical Diseases, Medical School, Nanjing University, Nanjing, China.
Huijie BianDepartment of Neurology, Nanjing Drum Tower Hospital, Medical School and The State Key Laboratory of Pharmaceutical Biotechnology, Institute of Translational Medicine for Brain Critical Diseases, Medical School, Nanjing University, Nanjing, China.
Yi LiuDepartment of Neurology, Nanjing Drum Tower Hospital, Medical School and The State Key Laboratory of Pharmaceutical Biotechnology, Institute of Translational Medicine for Brain Critical Diseases, Medical School, Nanjing University, Nanjing, China.
Meijuan ZhangDepartment of Neurology, Nanjing Drum Tower Hospital, Medical School and The State Key Laboratory of Pharmaceutical Biotechnology, Institute of Translational Medicine for Brain Critical Diseases, Medical School, Nanjing University, Nanjing, China.
Xiaolei ZhuDepartment of Neurology, Nanjing Drum Tower Hospital, Medical School and The State Key Laboratory of Pharmaceutical Biotechnology, Institute of Translational Medicine for Brain Critical Diseases, Medical School, Nanjing University, Nanjing, China.ORCID 0000-0003-4696-9696
Feng BaiDepartment of Neurology, Nanjing Drum Tower Hospital, Medical School and The State Key Laboratory of Pharmaceutical Biotechnology, Institute of Translational Medicine for Brain Critical Diseases, Medical School, Nanjing University, Nanjing, China.
Yun XuDepartment of Neurology, Nanjing Drum Tower Hospital, Medical School and The State Key Laboratory of Pharmaceutical Biotechnology, Institute of Translational Medicine for Brain Critical Diseases, Medical School, Nanjing University, Nanjing, China.ORCID 0000-0001-5288-0319
Nanjing Drum Tower Hospital · CNNanjing Brain Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pattern separation (PS) dysfunction is a type of cognitive impairment that presents early during the aging process, and this deficit has been attributed to structural and functional alterations in the dentate gyrus (DG) of the hippocampus. Absent in melanoma 2 (AIM2) is an essential component of the inflammasome. However, whether AIM2 plays a role in aging-associated cognitive dysfunction remains unclear. Here, we found that PS function was impaired in aging mice and was accompanied by marked synaptic loss and increased expression of AIM2 in the DG. Subsequently, we used an AIM2 overexpression virus and mice with AIM2 deletion to investigate the role of AIM2 in regulating PS function and synaptic plasticity and the mechanisms involved. Our study revealed that AIM2 regulates microglial activation during synaptic pruning in the DG region via the complement pathway, leading to impaired synaptic plasticity and PS function in aging mice. These results suggest a critical role for AIM2 in regulating synaptic plasticity and PS function and provide a new direction for ameliorating aging-associated cognitive dysfunction.

Indexed as

Cognitive DysfunctionAgingAnimalsDNA-Binding ProteinsInflammasomesMiceMicrogliaPhagocytosisAim2 protein, mouseDNA-Binding ProteinsInflammasomesagingAIM2complementmicrogliapattern separationsynaptic loss

Identifiers

PMID37177836
PMCPMC10352562
OpenAlexW4376504469

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.