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THE A53T MUTATION IN Α-SYNUCLEIN ENHANCES PROINFLAMMATORY ACTIVATION IN HUMAN MICROGLIA UPON INFLAMMATORY STIMULUS

Marine Krzischand 10 co-authors

Marine Krzisch

FENS Forum 2026 (2026)
Barcelona, Spain
Board PS03-08AM-068

Presentation

Date TBA

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Board: PS03-08AM-068

Poster preview

THE A53T MUTATION IN Α-SYNUCLEIN ENHANCES PROINFLAMMATORY ACTIVATION IN HUMAN MICROGLIA UPON INFLAMMATORY STIMULUS poster preview

Event Information

Poster Board

PS03-08AM-068

Abstract

Background: Parkinson’s disease (PD) is the second most common neurodegenerative disease, following Alzheimer’s. It is characterized by the aggregation of α-synuclein into Lewy bodies and Lewy neurites in the brain. Microglia-driven neuroinflammation may contribute to neuronal death in PD; however, the exact role of microglia remains unclear and has been understudied. The A53T mutation in the gene coding for α-synuclein has been linked to early-onset PD, and exposure to A53T mutant human α-synuclein increases the potential for inflammation of murine microglia. To date, its effect has not been studied in human microglia.
Methods: Here, we used 2-dimensional cultures of human pluripotent stem cell–derived microglia and transplantation of these cells into the mouse brain to assess the cell autonomous effects of the A53T mutation on human microglia.
Results: We found that A53T mutant human microglia had an intrinsically increased propensity toward proinflammatory activation upon inflammatory stimulus. Additionally, transplanted A53T mutant microglia showed a strong decrease in catalase expression in noninflammatory conditions and increased oxidative stress.
Conclusions: Our results indicate that A53T mutant human microglia display cell autonomous phenotypes that may worsen neuronal damage in early-onset PD.

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