Evidence map›Paper›PMID 37280314›Full record

ArticleJournal of neural transmission (Vienna, Austria : 1996)2023

The loss of function GBA1 c.231C > G mutation associated with Parkinson disease.

Dejie Chen, Yingchun Zheng, Guilian Zhang, Yuanbing Huang, Boyang Zheng, Jian Zhang, Fu Xiong, Quanxi Su

Abstract read
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In one paragraph

Article in Journal of neural transmission (Vienna, Austria : 1996), 2023. 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
0.5field-weighted citation impact, top 35% 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

0 citing papers in PubMed, 3 citations in OpenAlex.

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

8 authors at 5 institutions in 1 country.

Dejie Chen *Department of Neurology, Yunfu People's Hospital, Yunfu, China.
Yingchun Zheng *Department of Medical Genetics, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.ORCID 0000-0001-7902-6307
Guilian ZhangDepartment of Nephrology, Yunfu People's Hospital, Yunfu, China.
Yuanbing HuangDepartment of Neurology, Yunfu People's Hospital, Yunfu, China.
Boyang ZhengDepartment of Medical Genetics, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Jian ZhangDepartment of Medical Genetics, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Fu XiongDepartment of Medical Genetics, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China. xiongfu@smu.edu.cn.
Quanxi SuDepartment of Neurology, Yunfu People's Hospital, Yunfu, China. suquanxi@163.com.
Wenzhou Medical University · CNSouthern Medical University · CNCell Technology (China) · CNSun Yat-sen University · CNYuncheng University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parkinson's disease (PD) is the second most common neurodegenerative disease characterized by bradykinesia, rigidity, and tremor. However, familial PD caused by single-gene mutations remain relatively rare. Herein, we described a Chinese family affected by PD, which associated with a missense heterozygous glucocerebrosidase 1 (GBA1) mutation (c.231C > G). Clinical data on the proband and her family members were collected. Brain MRI showed no difference between affected and unaffected family members. Whole-exome sequencing (WES) was performed to identify the pathogenic mutation. WES revealed that the proband carried a missense mutation (c.231C > G) in GBA1 gene, which was considered to be associated with PD in this family. Sanger sequencing and co-segregation analyses were used to validate the mutation. Bioinformatics analysis indicated that the mutation was predicted to be damaging. In vitro functional analyses were performed to investigated the mutant gene. A decrease in mRNA and protein expression was observed in HEK293T cells transfected with mutant plasmids. The GBA1 c.231C > G mutation caused a decreased GBA1 concentration and enzyme activity. In conclusion, a loss of function mutation (c.231C > G) in GBA1 was identified in a Chinese PD family and was confirmed to be pathogenic through functional studies. This study help the family members understand the disease progression and provide a new example for studying the pathogenesis of GBA1-associated Parkinson disease.

Indexed as

Neurodegenerative DiseasesParkinson Diseasealpha-SynucleinFemaleGlucosylceramidaseHEK293 CellsHumansMutationalpha-SynucleinGlucosylceramidaseGBA1GCaseMutationParkinson’s diseaseWhole-exome sequencing

Identifiers

PMID37280314
OpenAlexW4379519646

What OpenQuestion holds

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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.