Evidence map›Paper›PMID 37773139›Full record

ArticleCell & bioscience2023

Neuronal MHC-I complex is destabilized by amyloid-β and its implications in Alzheimer's disease.

Min-Seok Kim, Kwangmin Cho, Mi-Hyang Cho, Na-Young Kim, Kyunggon Kim, Dong-Hou Kim, Seung-Yong Yoon

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

Article in Cell & bioscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 17% 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

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.

  1. Pooled it
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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

7 authors at 1 institution in 1 country.

Min-Seok Kim *ADEL Institute of Science & Technology (AIST), ADEL, Inc., Seoul, Korea.
Kwangmin Cho *ADEL Institute of Science & Technology (AIST), ADEL, Inc., Seoul, Korea.
Mi-Hyang ChoADEL Institute of Science & Technology (AIST), ADEL, Inc., Seoul, Korea.
Na-Young KimADEL Institute of Science & Technology (AIST), ADEL, Inc., Seoul, Korea.
Kyunggon KimDepartment of Convergence Medicine, Convergence Medicine Research Center/Biomedical Research Center, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
Dong-Hou KimDepartment of Brain Science, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea. dhkim@amc.seoul.kr.
Seung-Yong YoonADEL Institute of Science & Technology (AIST), ADEL, Inc., Seoul, Korea. ysy@amc.seoul.kr.ORCID http://orcid.org/0000-0003-0325-9993
Ulsan College · KR

Funding

Asan Institute for Life Sciences, Asan Medical Center 2019IL0067Ministry of Science, ICT and Future Planning 2018R1A2A1A05077403
6 · The paper itself

Abstract

backgroundsThe expression of major histocompatibility complex I (MHC-I) in neurons has recently been shown to regulate neurite outgrowth and synaptic plasticity. However, its contribution to neurodegenerative diseases such as Alzheimer's disease (AD) remains largely unknown.

methodsIn this study, we investigated the relationship between impaired MHC-I-β2M complex and AD in vitro and human AD samples. Interaction between protein was identified by liquid chromatography-tandem mass spectrometry and confirmed by immunoprecipitation. Single-chain trimer of MHC-I-β2M was generated to study the effect of stabilization of MHC-I-β2M complex on NCAM1 signaling.

resultsMHC-I is destabilized in the brains of AD patients and neuronal cells treated with oligomeric β-amyloid (Aβ). Specifically, Aβ oligomers disassemble the MHC-I-β2-microglobulin (β2M) complex, leading to reduced interactions with neural cell adhesion molecule 1 (NCAM1), a novel interactor of neuronal MHC-I, and decreased signaling. Inhibition of MHC-I-β2M complex destabilization by non-dissociable MHC-I-β2M-peptide complex restored MHC-I-NCAM1 signaling in neuronal cells.

conclusionsThe current study demonstrated that disruption of MHC-1-NCAM1 signaling by Aβ induced disassembly of MHC-I-β2M complex is involved in the pathophysiology of AD. Moreover, our findings suggest modulation of MHC-I stability may be a potential therapeutic target for restoring synaptic function in AD.

Indexed as

Alzheimer’s diseaseAmyloid-βHigh affinity peptideMHC-INCAM1β2-microglobulin

Identifiers

PMID37773139
PMCPMC10540404
OpenAlexW4387171978

What OpenQuestion holds

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LicenceCC BY
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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.