Evidence map›Paper›PMID 41388030›Full record

ArticleNPJ Parkinson's disease2025

Long-term oral glucocerebrosidase activator reduces soluble α-synuclein oligomer accumulation in Parkinsonian LRRK2 mutant mouse brain.

Zoe Yuen-Kiu Choi, Huifang Liu, Eunice Eun-Seo Chang, Shirley Yin-Yu Pang, Ivy Lingyi Luo, Yuefei Ruan, Qi Wang, Yasine Malki, Steffi Xi-Yue Zhang, Kerry Yupeng Weng and 5 more

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Article in NPJ Parkinson's disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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

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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

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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

15 authors.

Zoe Yuen-Kiu Choi *Department of Rehabilitation Sciences, Faculty of Health and Social Sciences, The Hong Kong Polytechnic University, Hong Kong SAR, China.
Huifang Liu *Department of Rehabilitation Sciences, Faculty of Health and Social Sciences, The Hong Kong Polytechnic University, Hong Kong SAR, China.
Eunice Eun-Seo ChangDepartment of Rehabilitation Sciences, Faculty of Health and Social Sciences, The Hong Kong Polytechnic University, Hong Kong SAR, China.
Shirley Yin-Yu PangDivision of Neurology, Department of Medicine, School of Clinical Medicine, University of Hong Kong, Hong Kong SAR, China.
Ivy Lingyi LuoDepartment of Rehabilitation Sciences, Faculty of Health and Social Sciences, The Hong Kong Polytechnic University, Hong Kong SAR, China.
Yuefei RuanState Key Laboratory of Marine Environmental Health (SKLMEH) and Department of Chemistry, City University of Hong Kong, Hong Kong SAR, China.
Qi WangState Key Laboratory of Marine Environmental Health (SKLMEH) and Department of Chemistry, City University of Hong Kong, Hong Kong SAR, China.
Yasine MalkiDivision of Neurology, Department of Medicine, School of Clinical Medicine, University of Hong Kong, Hong Kong SAR, China.
Steffi Xi-Yue ZhangDivision of Neurology, Department of Medicine, School of Clinical Medicine, University of Hong Kong, Hong Kong SAR, China.
Kerry Yupeng WengDepartment of Rehabilitation Sciences, Faculty of Health and Social Sciences, The Hong Kong Polytechnic University, Hong Kong SAR, China.
Benson Wui-Man LauDepartment of Rehabilitation Sciences, Faculty of Health and Social Sciences, The Hong Kong Polytechnic University, Hong Kong SAR, China.
Roy Chun-Laam NgDivision of Neuroscience, School of Biological Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, The University of Manchester, Manchester, M13 9PT, United Kingdom.
Zaijun ZhangGuangdong Province Key Laboratory of Pharmacodynamic, Constituents of TCM and New Drugs Research, Institute of New Drug Research, College of Pharmacy, Jinan University, Guangzhou, China.
Shu-Leong HoDivision of Neurology, Department of Medicine, School of Clinical Medicine, University of Hong Kong, Hong Kong SAR, China.
Philip Wing-Lok HoDepartment of Rehabilitation Sciences, Faculty of Health and Social Sciences, The Hong Kong Polytechnic University, Hong Kong SAR, China. philip-wl.ho@polyu.edu.hk.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Brain accumulation of toxic soluble α-synuclein (α-syn) oligomers represents a prodromal marker of synucleinopathies in Parkinson's disease (PD), contributing to progressive nigrostriatal neurodegeneration. Dysfunction in beta-glucocerebrosidase (GCase) and leucine-rich repeat kinase 2 (LRRK2) mutation are genetic risks for developing synucleinopathies. However, whether pharmacological GCase activation ameliorated synucleinopathies in LRRK2-PD was unexplored. Here, we showed that long-term treatment of ambroxol (ABX), a brain-penetrant GCase activator, reduced α-syn oligomer accumulation in aged mutant LRRK2

Identifiers

PMID41388030
PMCPMC12749452

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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.