Project description
Influenza infection as a trigger for Parkinson’s disease
Epidemiological studies suggest that influenza infection increases the risk of developing Parkinson’s disease. However, the underlying cellular mechanisms are unknown. With the support of the Marie Skłodowska-Curie Actions programme, the H1N1-BAM-PD project aims to investigate how the brain border immune compartment contributes to neurodegenerative risk following infection. Brain border immune cells reside at the interface between the brain and the rest of the body and may be a link between viral infection and neurodegeneration. Researchers will characterise how these cells respond to influenza infection and whether this response promotes the neuroinflammation and protein aggregation characteristic of Parkinson’s disease. Findings from mouse models will be complemented by analysis of immune signatures in patients.
Objective
Parkinson’s disease (PD) is the fastest-growing neurodegenerative disease worldwide, characterized by the accumulation of α-synuclein (αSyn). Evidence suggests two potential origins of αSyn pathology: brain-first or body-first initiation, with infection as possible trigger. Epidemiological studies implicate influenza infection in increasing the risk of developing PD, but the precise cellular mechanisms remain unclear. I propose that border-associated macrophages (BAMs), residing at the interface between the brain and periphery, are key to this question.
BAMs are pivotal regulators of neuroimmune responses at the brain borders, capable of sensing and responding to peripheral inflammatory cues. During brain viral infections, they promote immune cell recruitment and limit viral spread, while αSyn overexpression induces neuroinflammation, with BAM depletion reducing dopaminergic neurodegeneration.
I hypothesize that following influenza infection, BAMs sustain cytokine production and immune cell recruitment, which over time may promote neuroinflammation, αSyn propagation, and neurodegeneration in PD. Specifically, my research objectives are to:
1. Characterize the phenotype and function of brain border immune populations in mouse models of brain-first vs body-first PD.
2. Determine how BAMs respond to influenza infection and whether this affects neurodegeneration later in life.
3. Identify peripheral immune signatures in prodromal PD patients stratified by severe infection, to detect potential populations trafficking to the brain and increasing PD risk.
By combining my expertise in viral immunology with Dr. De Schepper’s PD research and Dr. Delputte’s virology expertise, this interdisciplinary project aims to move beyond the current state-of-the-art to elucidate how influenza infection increases PD risk at the brain borders.
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Project’s keywords as indicated by the project coordinator. Not to be confused with the EuroSciVoc taxonomy (Fields of science)
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HORIZON.1.2 - Marie Skłodowska-Curie Actions (MSCA)
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HORIZON-TMA-MSCA-PF-EF - HORIZON TMA MSCA Postdoctoral Fellowships - European Fellowships
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(opens in new window) HORIZON-MSCA-2025-PF
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9052 ZWIJNAARDE - GENT
Belgium
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