ArticleJournal of movement disorders2026
Cardiac 123I-Meta-Iodobenzylguanidine Imaging as a Biomarker for Body-First Parkinson's Disease: Linking Peripheral α-Synuclein to Clinical Subtyping.
Article in Journal of movement disorders, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
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.
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Who cites it
3 citing papers in PubMed.
- Equivocal Dopamine Transporter Imaging: Integrating Visual Assessment, Quantification, and Clinical Follow-Up.Life (Basel, Switzerland) · 2026Review
- Clinical Significance of Thyroid 123I- Meta-Iodobenzylguanidine Uptake in Parkinson's Disease.Journal of movement disorders · 2026Article
- Human and Mouse Alpha-Synuclein Fibrillation: Impact on h-FTAA Binding and Advancing Strain-Specific Biomarkers in PD Animal Models.International journal of molecular sciences · 2026Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Recent neuropathological and imaging studies support the concept of "brain-first vs. body-first" Parkinson's disease (PD), which is based on the α-synuclein origin site and connectome model. The body-first phenotype is characterized by early involvement of the peripheral autonomic nervous system, particularly the cardiac sympathetic nerves and enteric nerves. 123I-meta-iodobenzylguanidine (123I-MIBG) myocardial scintigraphy is a well-established method for evaluating cardiac sympathetic innervation. This review explores the potential of 123I-MIBG scintigraphy as a biomarker to differentiate the body-first phenotype from the brain-first phenotype. Reduced 123I-MIBG uptake has been observed in idiopathic rapid eye movement (REM) sleep behavior disorder, pure autonomic failure, and incidental Lewy body disease-conditions strongly associated with prodromal or early-stage PD. Postmortem and biopsy evidence indicates α-synuclein accumulation in cardiac nerves and other peripheral sites, which is consistent with bottom-up progression. α-Synuclein seed amplification assays further corroborate the association between the peripheral α-synuclein burden and reduced 123I-MIBG uptake. While 123I-MIBG myocardial scintigraphy is a promising tool, its limitations include cost, limited availability, and potential confounding from underlying cardiac conditions. Nonetheless, early detection of cardiac sympathetic denervation via 123I-MIBG imaging may enhance diagnosis, support subtype classification, and improve the understanding of PD pathogenesis.
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Registered trials
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 Socratic graph.