Evidence map›Paper›PMID 41667769›Full record

ArticleJournal of neurology2026

Neuronal antibody targeting metabotropic glutamate receptor 8 in five cases and its pathogenicity.

Pei-Hao Lin, Shi-Feng Zhang, Hai-Yan Yao, Wen-Dong Lai, Shi-Yu He, Shi-Chun Li, Hui-Lu Li, Zhan-Hang Wang, Dong-Fang Cao, Jie Yang and 7 more

Abstract read
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In one paragraph

Article in Journal of neurology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

17 authors.

Pei-Hao Lin *Department of Neurology, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, Institute of Neuroscience, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.
Shi-Feng Zhang *Department of Neurology, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, Institute of Neuroscience, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.
Hai-Yan Yao *Department of Neurology, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, Institute of Neuroscience, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.
Wen-Dong LaiDepartment of Neurology, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, Institute of Neuroscience, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.
Shi-Yu HeDepartment of Neurology, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, Institute of Neuroscience, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.
Shi-Chun LiDepartment of Neurology, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, Institute of Neuroscience, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.
Hui-Lu LiDepartment of Neurology, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China.
Zhan-Hang WangDepartment of Neurology, Guangdong Sanjiu Brain Hospital, Guangzhou, China.
Dong-Fang CaoDepartment of Neurology, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, Institute of Neuroscience, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.
Jie YangDepartment of Neurology, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, Institute of Neuroscience, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.
Li HuangDepartment of Neurology, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, Institute of Neuroscience, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.
Ting LiDepartment of Neurology, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, Institute of Neuroscience, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.
Cong GaoDepartment of Neurology, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, Institute of Neuroscience, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.
Cong-Cong FuDepartment of Neurology, Guangzhou Eighth People's Hospital, Guangzhou Medical University, Guangzhou, China.
An-Lin CaiDepartment of Neurology, Guangdong Second Provincial General Hospital, Guangzhou, China.
Li MaDepartment of Neurology, Yan'an University Affiliated Hospital, Yan'an, China. 1325569197@qq.com.
You-Ming LongDepartment of Neurology, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, Institute of Neuroscience, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, China. youminglong@126.com.ORCID http://orcid.org/0000-0002-4004-2948

Funding

Basic and Applied Basic Research Foundation of Guangdong Province 2022A1515110143Basic and Applied Basic Research Foundation of Guangdong Province 2023A1515010225
6 · The paper itself

Abstract

objectiveTo characterize patients with autoantibodies against metabotropic glutamate receptor 8 (mGluR8) and assess the pathogenicity of these antibodies.

methodsAnti-mGluR8 antibodies were detected via cell-based assay and immunoprecipitation. Clinical data from five anti-mGluR8-positive patients and previously reported cases with other anti-mGluR antibodies were reviewed. Patient-derived IgG was purified and absorbed using mGluR8-expressing or control HEK293T cells. Pathogenicity was tested in hippocampal neuron cultures and via passive transfer into mice, with ataxia evaluated using behavioral tests.

resultsFive patients (4 male, median age 61) presented with subacute ataxia; other symptoms included dysarthria, ophthalmoplegia, dysphagia, and cognitive changes. Brain MRI showed cerebellar and cortical atrophy in all cases. Immunotherapy led to transient improvement in all patients, with stabilization in three of four with follow-up. In vitro, non-mGluR8-absorbed IgG reduced synaptic mGluR8 clusters. Mice injected with non-mGluR8-absorbed IgG developed transient ataxia peaking at 3-6 h and resolving within 24 h, correlating with antibody binding to Purkinje cells.

conclusionAnti-mGluR8 antibody is a novel possible biomarker for autoimmune ataxia, with its pathogenicity supported by passive transfer models.

Indexed as

AutoantibodiesAutoimmune Diseases of the Nervous SystemCerebellar AtaxiaNeuronsReceptors, Metabotropic GlutamateAgedAnimalsFemaleHEK293 CellsHumansImmunization, PassiveImmunoglobulin GMaleMiceMiddle AgedAutoantibodiesImmunoglobulin GReceptors, Metabotropic GlutamateAnti-mGluR8 antibodyAutoimmune disorderCerebellar ataxiaPassive transfer model

Identifiers

PMID41667769

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