ReviewJournal of neural transmission (Vienna, Austria : 1996)2023
The brain-first vs. body-first model of Parkinson's disease with comparison to alternative models.
Review 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. Cited by 56 papers.
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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.
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Who cites it
56 citing papers in PubMed, 86 citations in OpenAlex.
- Anatomy and function of efferent and afferent vagal innervation of the stomach.Autonomic neuroscience : basic & clinical · 2026Review
- Association between cerebrospinal fluid LRRK2 and incident orthostatic hypotension differs by genetic background in Parkinson's disease.Acta neurologica Belgica · 2026Article
- Brain-first and body-first subtypes of Lewy body disease.Nature reviews. Neurology · 2026Review
- Neurons Die Not by One Hit, but by Signaling Convergence.Molecular neurobiology · 2026Review
- Co- and Multi-Pathologies in Parkinson's Disease: An International Parkinson and Movement Disorder Society Scientific Issues Committee Review.Movement disorders : official journal of the Movement Disorder Society · 2026Review
- The German Parkinson expert meetings.Journal of neural transmission (Vienna, Austria : 1996) · 2026Article
- Brain-first versus body-first Parkinson's disease: Differential findings on pupillary, brainstem and vagus sonography.Journal of neurology · 2026Article
- Article
- Case report of Parkinson's disease in isolated congenital anosmia with absent olfactory bulbs.NPJ Parkinson's disease · 2026Article
- Brain-First vs. Body-First Models in Neurodegenerative Disease: A Perspective Review.NeuroSci · 2026Review
- Temporal onset of non-motor symptoms and the body-first/brain-first dichotomy in Parkinson's disease: a cross-sectional single center experience.Journal of neural transmission (Vienna, Austria : 1996) · 2026Article
- Focused Ultrasound for the Treatment of Circuit and Molecular Pathology in Parkinson's Disease.Movement disorders : official journal of the Movement Disorder Society · 2026Review
- A Pathophysiological Model of Parkinson's Disease Based on Microvascular Flow Disturbance and Leukocyte-Mediated Oxidative Injury in Critical Pigmented Neuronal Niches.Antioxidants (Basel, Switzerland) · 2026Article
- Prodromal Lewy Body Symptoms and α-Synuclein Seeding in Idiopathic Olfactory Dysfunction.Movement disorders clinical practice · 2026Article
- Characteristics and mechanisms of cognitive impairment in Parkinson disease.Nature reviews. Neurology · 2026Review
- Striatal (a-)symmetry reveals sex-specific autonomic vulnerabilities in early Parkinson's disease.npj women's health · 2026Article
- Amygdala subregion MRI alterations in Parkinson's disease correlate with olfactory function.Frontiers in aging neuroscience · 2026Article
- Brain metabolic and network profiles characterized by comorbid depressive symptoms and sleep disturbances in Parkinson's disease: anFrontiers in aging neuroscience · 2026Article
- Basal Forebrain Volume Predicts Disease Conversion in Prodromal Synucleinopathy.Movement disorders clinical practice · 2026Article
- Functional Magnetic Resonance Imaging (fMRI) Signatures of Progression and Phenoconversion in Prodromal Synucleinopathies.Movement disorders : official journal of the Movement Disorder Society · 2025Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
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Abstract
The ultimate origin of Lewy body disorders, including Parkinson's disease (PD) and Dementia with Lewy bodies (DLB), is still incompletely understood. Although a large number of pathogenic mechanisms have been implicated, accumulating evidence support that aggregation and neuron-to-neuron propagation of alpha-synuclein may be the core feature of these disorders. The synuclein, origin, and connectome (SOC) disease model of Lewy body disorders was recently introduced. This model is based on the hypothesis that in the majority of patients, the first alpha-synuclein pathology arises in single location and spreads from there. The most common origin sites are the enteric nervous system and the olfactory system. The SOC model predicts that gut-first pathology leads to a clinical body-first subtype characterized by prodromal autonomic symptoms and REM sleep behavior disorder. In contrast, olfactory-first pathology leads to a brain-first subtype with fewer non-motor symptoms before diagnosis. The SOC model further predicts that body-first patients are older, more commonly develop symmetric dopaminergic degeneration, and are at increased risk of dementia-compared to brain-first patients. In this review, the SOC model is explained and compared to alternative models of the pathogenesis of Lewy body disorders, including the Braak staging system, and the Unified Staging System for Lewy Body Disorders. Postmortem evidence from brain banks and clinical imaging data of dopaminergic and cardiac sympathetic loss is reviewed. It is concluded that these datasets seem to be more compatible with the SOC model than with those alternative disease models of Lewy body disorders.
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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.