ePoster

DISSECTING TAU SPREADING IN A HUMAN MICROFLUIDIC MICROGLIA–NEURON CO-CULTURE SYSTEM

Bruno Queirósand 6 co-authors

Univ. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1167 - RID-AGE

FENS Forum 2026 (2026)
Barcelona, Spain
Board PS02-07PM-382

Presentation

Date TBA

Board: PS02-07PM-382

Poster preview

DISSECTING TAU SPREADING IN A HUMAN MICROFLUIDIC MICROGLIA–NEURON CO-CULTURE SYSTEM poster preview

Event Information

Poster Board

PS02-07PM-382

Abstract

Tau protein is a key element of neuronal structure and function, but under pathological conditions such as Alzheimer’s disease (AD), it can misfold, aggregate, and pathological strains can propagate, leading to synaptic dysfunction and neuronal loss. Tau spreading follows a prion-like mechanism involving a self-propagating autocatalytic manner of spreading and templated seeding influenced by its size, isoform, mutations, and post-translational modifications. Microglia further modulate Tau pathology by affecting Tau modifications, aggregation, intercellular transfer, and driving neuroinflammatory signaling. Despite these insights, the combined effects of Tau’s intrinsic molecular properties and microglial activity on Tau spreading and disease progression remain poorly understood.
To investigate the mechanisms underlying Tau spreading, we established a microfluidic co-culture system combining human induced microglia (iMCG), Tau-/- neurons, and astrocytes. The microfluidic devices consist of three neuronal chambers interconnected by microchannels that permit unidirectional axonal growth from the first to second and then third compartment while preventing reverse connectivity. This design enables selective Tau overexpression in a defined neuronal population and controlled assessment of its propagation to downstream compartments. Ultimately, establishing a co-culture model with iMCG derived from human pluripotent stem cells platform enables neuronal compartmentalization permitting precise control and detailed analysis of Tau spreading capacity, clearance mechanisms, and neuron–microglia interactions.

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