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EXPLORING GUT-BRAIN CROSSTALK IN PARKINSON’S DISEASE PATHOGENESIS USING HUMAN-INDUCED PLURIPOTENT STEM CELL MODELS
Tanya Singhand 3 co-authors
University of Oxford
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS03-08AM-053
Presentation
Date TBA
Board: PS03-08AM-053
Event Information
Poster Board
PS03-08AM-053
Poster
View posterAbstract
Parkinson’s disease (PD) is a progressive neurodegenerative disorder with no curative treatment. Clinically, PD is typically diagnosed only after motor symptoms emerge, by which point substantial loss of dopaminergic neurons in the substantia nigra has already occurred. Consequently, the earliest disease-driving processes remain poorly understood. Increasing evidence suggests that PD pathology may originate outside the brain, particularly in the gastrointestinal (GI) tract, before spreading to the central nervous system via the vagus nerve. Supporting this idea, non-motor symptoms such as GI dysfunction often precede movement impairments by years, and pathological α-synuclein can be detected in gut tissue during prodromal stages. Mutations in the GBA1 gene, the most common genetic risk factor for PD, are linked to earlier disease onset, accelerated α-synuclein accumulation, and more severe progression. However, the mechanisms connecting gut pathology to brain dysfunction remain poorly understood, highlighting the need for human-relevant models that capture both early gut and brain changes. To address this gap, we generated ventral midbrain organoids and enteric nervous system (ENS) models from human induced pluripotent stem cells derived from control and GBA1 mutation lines. While controls developed expected neural identities, GBA1 mutants exhibited altered gene expression and increased spontaneous neuronal activity, indicative of disrupted neural network function. ENS models showed changes in genes involved in early enteric development, suggesting impaired neurogenesis that may contribute to early GI symptoms. Future work will integrate these systems using a microfluidic brain-on-chip platform to study gut-brain interactions in a controlled human model.
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