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Positron emission tomography tracers for synucleinopathies
Jie Xiang, Zhentao Zhang, Shengxi Wu, Keqiang Ye. Molecular Neurodegeneration, 2025-01-05
Topic: Brain proteins, microglia and lab models
Synucleinopathies, such as Parkinson's disease, dementia with Lewy bodies, and multiple system atrophy, are characterized by the aggregation of α-synuclein. Variations in brain distribution allow for differentiation among these diseases and facilitate precise clinical diagnosis. However, distinguishing between synucleinopathies and Parkinsonism with tauopathies poses a challenge, significantly impacting clinical drug development. Therefore, molecular imaging is crucial for synucleinopathies, particularly for clinical diagnosis, assessment of drug efficacy, and disease surveillance. In recent years, advances in molecular imaging have led to rapid development of α-synuclein-specific tracers for positron emission tomography (PET), most of which are still in pre-clinical stages. Interestingly, some of these tracers share similar compound skeletal structures and are currently undergoing optimization for clinical application. Despite this progress, there remain challenges in developing α-synuclein tracers. This review summarizes recent findings on promising PET tracers and discusses representative compounds' characteristics while offering suggestions for further research orientation.
Key findings
- However, distinguishing between synucleinopathies and Parkinsonism with tauopathies poses a challenge, significantly impacting clinical drug development.
Why it matters
This review summarizes progress on PET tracers for alpha-synuclein, noting that most are still in pre-clinical stages and that distinguishing synucleinopathies from tauopathies remains difficult. It concerns imaging tools for diagnosis and drug development, not a treatment, cure, or prevention.
Study details
- Evidence strengthLow
How this study scored 47/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Molecular Neurodegeneration) |
| Journal's citation record | 2 / 4 | Molecular Neurodegeneration: journal h-index 164 (OpenAlex, 2026-10-29) |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 4 / 5 | 2025 — within 3 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 3 / 7 | Cited 25 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 8.3 citations a year over 3 year(s) since 2025 |
| Impact for its field and year | 4 / 6 | Cited 14.1× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 0 / 6 | No other study in this library cites it |
| Still being cited | 2 / 4 | Cited 25 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Keqiang Ye: h-index 82 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | Chinese Academy of Sciences: institution h-index 1,801 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 5 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 39757220) |
| Free to read | 2 / 2 | Free to read |
| Total | 47 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1186/s13024-024-00787-9
- PubMed: 39757220
- Original source →
- Free full text: Molecular Neurodegeneration →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.
APA 7th
Xiang, J., Zhang, Z., Wu, S., & Ye, K. (2025). Positron emission tomography tracers for synucleinopathies. Molecular Neurodegeneration. https://doi.org/10.1186/s13024-024-00787-9
Vancouver
Xiang J, Zhang Z, Wu S, Ye K. Positron emission tomography tracers for synucleinopathies. Molecular Neurodegeneration. 2025. doi:10.1186/s13024-024-00787-9. PMID: 39757220.
BibTeX
@article{xiang2025-39757220,
author = {Xiang, Jie and Zhang, Zhentao and Wu, Shengxi and Ye, Keqiang},
title = {{Positron emission tomography tracers for synucleinopathies}},
journal = {Molecular Neurodegeneration},
year = {2025},
doi = {10.1186/s13024-024-00787-9},
pmid = {39757220},
url = {https://doi.org/10.1186/s13024-024-00787-9}
}
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