Evidence map›Paper›PMID 38421467›Full record

ArticleMolecular neurobiology2024

IRAK-M Plays A Role in the Pathology of Amyotrophic Lateral Sclerosis Through Suppressing the Activation of Microglia.

Xinghua Zhong, Chuqiao Li, Yanran Li, Yingyi Huang, Jingsi Liu, Anqi Jiang, Jinyu Chen, Yu Peng

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed, 1 pooled it
0.4field-weighted citation impact, top 42% 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

1 citing paper in PubMed, 1 synthesis or guideline pooled it, 1 citations in OpenAlex.

  1. Pooled it
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

8 authors at 2 institutions in 1 country.

Xinghua Zhong *Department of Neurology, Nanfang Hospital, Southern Medical University, No. 1838, North Guangzhou Avenue, Guangzhou, 510515, Guangdong, China.
Chuqiao Li *Department of Neurology, Nanfang Hospital, Southern Medical University, No. 1838, North Guangzhou Avenue, Guangzhou, 510515, Guangdong, China.
Yanran LiDepartment of Neurology, Nanfang Hospital, Southern Medical University, No. 1838, North Guangzhou Avenue, Guangzhou, 510515, Guangdong, China.
Yingyi HuangDepartment of Neurology, Nanfang Hospital, Southern Medical University, No. 1838, North Guangzhou Avenue, Guangzhou, 510515, Guangdong, China.
Jingsi LiuDepartment of Neurology, Nanfang Hospital, Southern Medical University, No. 1838, North Guangzhou Avenue, Guangzhou, 510515, Guangdong, China.
Anqi JiangDepartment of Neurology, Nanfang Hospital, Southern Medical University, No. 1838, North Guangzhou Avenue, Guangzhou, 510515, Guangdong, China.
Jinyu ChenDepartment of Neurology, Nanfang Hospital, Southern Medical University, No. 1838, North Guangzhou Avenue, Guangzhou, 510515, Guangdong, China. chenjinyu0218@163.com.
Yu PengDepartment of Neurology, Nanfang Hospital, Southern Medical University, No. 1838, North Guangzhou Avenue, Guangzhou, 510515, Guangdong, China. pengyu_smu@163.com.ORCID http://orcid.org/0009-0008-5014-3997
Nanfang Hospital · CNGuangzhou First People's Hospital · CN

Funding

National Natural Science Foundation of China 81901239National Natural Science Foundation of China 82171354Science and Technology Projects in Guangzhou 202201010924
6 · The paper itself

Abstract

Microglial activation plays a crucial role in the disease progression in amyotrophic lateral sclerosis (ALS). Interleukin receptor-associated kinases-M (IRAK-M) is an important negative regulatory factor in the Toll-like receptor 4 (TLR4) pathway during microglia activation, and its mechanism in this process is still unclear. In the present study, we aimed to investigate the dynamic changes of IRAK-M and its protective effects for motor neurons in SOD1-G93A mouse model of ALS. qPCR (Real-time Quantitative PCR Detecting System) were used to examine the mRNA levels of IRAK-M in the spinal cord in both SOD1-G93A mice and their age-matched wild type (WT) littermates at 60, 100 and 140 days of age. We established an adeno-associated virus 9 (AAV9)-based platform by which IRAK-M was targeted mostly to microglial cells to investigate whether this approach could provide a protection in the SOD1-G93A mouse. Compared with age-matched WT mice, IRAK-M mRNA level was elevated at 100 and 140 days in the anterior horn region of spinal cords in the SOD1-G93A mouse. AAV9-IRAK-M treated SOD1-G93A mice showed reduction of IL-1β mRNA levels and significant improvements in the numbers of spinal motor neurons in spinal cord. Mice also showed previously reduction of muscle atrophy. Our data revealed the dynamic changes of IRAK-M during ALS pathological progression and demonstrated that an AAV9-IRAK-M delivery was an effective and translatable therapeutic approach for ALS. These findings may help identify potential molecular targets for ALS therapy.

Indexed as

Amyotrophic Lateral SclerosisInterleukin-1 Receptor-Associated KinasesMice, TransgenicMicrogliaSpinal CordAnimalsDependovirusDisease Models, AnimalHumansInterleukin-1betaMiceMice, Inbred C57BLMotor NeuronsRNA, MessengerSuperoxide Dismutase-1Interleukin-1betaInterleukin-1 Receptor-Associated KinasesRNA, MessengerSuperoxide Dismutase-1Amyotrophic lateral sclerosis(ALS)Interleukin receptor-associated kinases-M (IRAK-M)MicrogliaSOD1-G93A mice

Identifiers

PMID38421467
OpenAlexW4392292673

What OpenQuestion holds

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Registered trials

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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.