Evidence map›Paper›PMID 38589016›Full record

ArticleJournal of movement disorders2024

α-Synuclein: A Promising Biomarker for Parkinson's Disease and Related Disorders.

Taku Hatano, Ayami Okuzumi, Gen Matsumoto, Taiji Tsunemi, Nobutaka Hattori

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of movement disorders, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing 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

27 citing papers in PubMed.

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  18. Vascular parkinsonism: an update.Journal of neural transmission (Vienna, Austria : 1996) · 2025
    Review
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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

5 authors.

Taku HatanoDepartment of Neurology, Juntendo University Faculty of Medicine, Tokyo, Japan.
Ayami OkuzumiDepartment of Neurology, Juntendo University Faculty of Medicine, Tokyo, Japan.
Gen MatsumotoDepartment of Histology and Cell Biology, Nagasaki University School of Medicine, Nagasaki, Japan.
Taiji TsunemiDepartment of Neurology, Juntendo University Faculty of Medicine, Tokyo, Japan.
Nobutaka HattoriDepartment of Neurology, Juntendo University Faculty of Medicine, Tokyo, Japan.

Funding

Health, Labor, and Welfare Sciences Research GrantsJapan Agency for Medical Research and Development 20dm0107156Japan Agency for Medical Research and Development 21ak0101112Japan Agency for Medical Research and Development 23dk0207055Japan Agency for Medical Research and Development 23dm0207070Japan Agency for Medical Research and Development 23wm0425015Japan Agency for Medical Research and Development 23wm0425019Japan Society for the Promotion of ScienceMinistry of Health, Labour and WelfareResearch Committee of CNS Degenerative DiseaseScientific Research 19K16928Scientific Research 21H04820Scientific Research 21K07424Scientific Research 21K08742Visionary Council JPMJMS2024-5
6 · The paper itself

Abstract

Mutations in the SNCA gene, which encodes α-synuclein (α-syn), play a key role in the development of genetic Parkinson's disease (PD). α-Syn is a major component of Lewy bodies in PD and glial cytoplasmic inclusions in multiple system atrophy (MSA). Rapid eye movement sleep behavior disorder patients often progress to PD, dementia with Lewy bodies, or MSA, which are collectively known as α-synucleinopathies. The loss of dopaminergic neurons with Lewy bodies precedes motor dysfunction in these diseases, but the mechanisms of neurodegeneration due to α-syn aggregation are poorly understood. Monitoring α-syn aggregation in vivo could serve as a diagnostic biomarker and help elucidate pathogenesis, necessitating a simple and accurate detection method. Seed amplification assays (SAAs), such as real-time quaking-induced conversion and protein misfolding cyclic amplification, are used to detect small amounts of abnormally structured α-syn protofibrils, which are central to aggregation. These methods are promising for the early diagnosis of α-synucleinopathy. Differences in α-syn filament structures between α-synucleinopathies, as observed through transmission electron microscopy and cryo-electron microscopy, suggest their role in the pathogenesis of neurodegeneration. SAAs may differentiate between subtypes of α-synucleinopathy and other diseases. Efforts are also being made to identify α-syn from blood using various methods. This review introduces body fluid α-syn biomarkers based on pathogenic α-syn seeds, which are expected to redefine α-synucleinopathy diagnosis and staging, improving clinical research accuracy and facilitating biomarker development.

Indexed as

Multiple system atrophyParkinson’s diseaseSeed amplification assaysα-Synucleinα-Synucleinopathy

Identifiers

PMID38589016
PMCPMC11082597

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.