α-Synuclein in gut endocrine cells and its implications for Parkinson’s disease
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Parkinson’s disease (PD) is a progressive neurodegenerative disease with devastating clinical manifestations. In PD, neuronal death is associated with intracellular aggregates of the neuronal protein α-synuclein known as Lewy bodies. Although the cause of sporadic PD is not well understood, abundant clinical and pathological evidence show that misfolded α-synuclein is found in enteric nerves before it appears in the brain. This suggests a model in which PD pathology originates in the gut and spreads to the central nervous system via cell-to-cell prion-like propagation, such that transfer of misfolded α-synuclein initiates misfolding of native α-synuclein in recipient cells. We recently discovered that enteroendocrine cells (EECs), which are part of the gut epithelium and directly face the gut lumen, also possess many neuron-like properties and connect to enteric nerves. In this report, we demonstrate that α-synuclein is expressed in the EEC line, STC-1, and native EECs of mouse and human intestine. Furthermore, α-synuclein–containing EECs directly connect to α-synuclein–containing nerves, forming a neural circuit between the gut and the nervous system in which toxins or other environmental influences in the gut lumen could affect α-synuclein folding in the EECs, thereby beginning a process by which misfolded α-synuclein could propagate from the gut epithelium to the brain.
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These cell types offer a theoretical source for early pathological α-synuclein aggregation and spread to the brain via the vagus nerve.
“Both cell types naturally express α-synuclein and offer a theoretical source for early pathological α-synuclein aggregation and spread to the brain via the vagus nerve [9, 137].”
From The gut–brain axis in early Parkinson’s disease: from prodrome to prevention (2025) · cites this paper as [137]
Gastrointestinal enteroendocrine cells and submucosal neurones could be sources of α-synuclein.
“Gastrointestinal enteroendocrine cells that connect directly to the gut lumen and local neurones, and submucosal neurones which synapse micrometers from the gut lumen, could also be sources of α-synuclein [137].”
From The gut–brain axis in early Parkinson’s disease: from prodrome to prevention (2025) · cites this paper as [137]
Both enteroendocrine cells and submucosal neurones naturally express α-synuclein.
“Both cell types naturally express α-synuclein and offer a theoretical source for early pathological α-synuclein aggregation and spread to the brain via the vagus nerve [9, 137].”
From The gut–brain axis in early Parkinson’s disease: from prodrome to prevention (2025) · cites this paper as [137]
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Parkinson's disease: Alterations in iron and redox biology as a key to unlock therapeutic strategies
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The gut microbiome and mental health: advances in research and emerging priorities
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Prion-Like Mechanisms in Parkinson’s Disease
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High fat diet induces microbiota-dependent silencing of enteroendocrine cells
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Invited Review: From nose to gut – the role of the microbiome in neurological disease
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Hydrogen Sulfide Produced by Gut Bacteria May Induce Parkinson’s Disease
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Parkinson’s progression prediction using machine learning and serum cytokines
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TLR2 and TLR4 in Parkinson’s disease pathogenesis: The environment takes a toll on the gut
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Role of enteric glia and microbiota-gut-brain axis in parkinson disease pathogenesis
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Visceral Inflammation and Immune Activation Stress the Brain
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The gut-brain axis and Parkinson disease: Clinical and pathogenetic relevance
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Self-citationGut–Brain Axis as a Pathological and Therapeutic Target for Neurodegenerative Disorders
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Diabesity and mood disorders: Multiple links through the microbiota-gut-brain axis
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Upregulation of α-synuclein following immune activation: Possible trigger of Parkinson's disease
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Animal models of brain-first and body-first Parkinson's disease
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Epidemiology of Parkinson’s Disease: An Update
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Neuroscience: A Distributed Neural Network Controls REM Sleep
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Neuroinflammation in neurodegeneration via microbial infections
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Ingestion of subthreshold doses of environmental toxins induces ascending Parkinsonism in the rat
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Gut mucosal cells transfer α-synuclein to the vagus nerve
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Self-citationIntestinal Enteroendocrine Cells: Present and Future Druggable Targets
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Can the gut be the missing piece in uncovering PD pathogenesis?
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Modulatory Effect of Gut Microbiota on the Gut-Brain, Gut-Bone Axes, and the Impact of Cannabinoids
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Gastrointestinal disorders in Parkinson’s disease and other Lewy body diseases
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Polystyrene Nanoplastics Hitch-Hike the Gut–Brain Axis to Exacerbate Parkinson’s Pathology
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Gastric emptying in Parkinson's disease – A mini-review
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What Is the Evidence that Parkinson’s Disease Is a Prion Disorder, Which Originates in the Gut?
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Digesting recent findings: gut alpha-synuclein, microbiome changes in Parkinson’s disease
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Rewiring the Brain Through the Gut: Insights into Microbiota–Nervous System Interactions
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<p>Colonic inflammation affects myenteric alpha-synuclein in nonhuman primates</p>
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Enteroendocrine cells: the gatekeepers of microbiome-gut-brain communication
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Molecular and Cellular Interactions in Pathogenesis of Sporadic Parkinson Disease
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“Both cell types naturally express α-synuclein and offer a theoretical source for early pathological α-synuclein aggregation and spread to the brain via the vagus nerve [9, 137].”
α‐Synuclein in Parkinson's Disease: From Bench to Bedside
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Distinct Bile Acid Signature in Parkinson's Disease With Mild Cognitive Impairment
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The gut-brain axis in Parkinson's disease
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Gut Microbiota and Disorders of the Central Nervous System
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Gut Bacteria Regulate the Pathogenesis of Huntington’s Disease in Drosophila Model
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Parkinson's Disease and the Gut: Models of an Emerging Relationship
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Update to the Treatment of Parkinson’s Disease Based on the Gut-Brain Axis Mechanism
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Lack of pathogenic potential of peripheral α-synuclein aggregates from Parkinson’s disease patients
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- Authors
- Chandra, R., Hiniker, A., Kuo, Y.-M., Nussbaum, R. L., & Liddle, R. A.
- Affiliations
- Duke University (US)
- Department of Pathology and
- University of California, San Francisco (US)
- Venue
- JCI Insight
- Published
- 2017-06-15
- Volume
- 2
- Issue
- 12
- ISSN
- 2379-3708 (ISSN-L)
- PMC
- PMC5470880
- OpenAlex
- W2626849072
- Cited by
- 236
- References
- 67
- Citations by year
- 2026: 22 · 2025: 26 · 2024: 28 · 2023: 26 · 2022: 43 · 2021: 28 · 2020: 15 · 2019: 20 · 2018: 23 · 2017: 4 · 2016: 1
- FWCI
- 12.00
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- JCI Insight (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- U.S. Department of Veterans Affairs (BX002230, I01 BX002230)
- Sandler Foundation
- National Institutes of Health (UL1TR001117)
- University of California, San Francisco
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK098796, R01DK109368)
- National Institute of Neurological Disorders and Stroke (K08NS090633)
- Duke Cancer Institute
- Topics
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- alpha-synuclein, Parkinson's disease, enteroendocrine cells, gut-brain axis, Lewy bodies, prion-like propagation, enteric nerves, STC-1 cells, neurodegeneration, intestinal epithelium
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