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Restoring microglial lysosomal capacity in neurodegeneration

Objective

Alzheimer’s disease (AD) is the most common cause of dementia, affecting over 57 million people worldwide. It is a progressive, fatal neurodegenerative disorder with no curative treatments, imposing a major burden on patients, families, healthcare systems, and society.
AD is marked by amyloid-beta (Aβ) plaque accumulation. Microglia, the brain’s immune cells, attempt to degrade these aggregates through their lysosomes, but this process is often inefficient and may even contribute to Aβ spread.
I hypothesize that Aβ pathology reshapes the proteome of human microglial lysosomes, impairing their function and promoting disease progression. To date, no study has systematically mapped how the human microglial lysosomal proteome changes dynamically in response to Aβ pathology.
To address this knowledge gap, I will use a xenotransplantation model in which human iPSC-derived microglia are engrafted into either healthy or Aβ-accumulating mouse brains. TurboID proximity labeling will enable in vivo profiling of lysosomal proteins altered by Aβ pathology. To test the functional consequences of this alteration, I will employ a targeted CRISPR/Cas9 screen in human microglia-neuron-astrocyte tri-cultures, identifying genes whose disruption enhances Aβ clearance. Promising candidates will be then validated in vivo using antisense oligonucleotides.
The host laboratory has established the xenotransplantation model, the TurboID system, and the CRISPR platform, while I bring extensive expertise in human tri-cultures. I therefore believe that this makes an unprecedented opportunity to move beyond the state of the art and address a major gap in AD research.
The project will generate the first in vivo map of the human microglial lysosomal proteome under Aβ pathology, uncovering candidate therapeutic targets to restore clearance. In doing so, it will open new avenues to modify AD and other neurodegenerative disorders where protein accumulation and microglia dysfunction are key drivers.

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HORIZON-TMA-MSCA-PF-EF - HORIZON TMA MSCA Postdoctoral Fellowships - European Fellowships

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Call for proposal

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(opens in new window) HORIZON-MSCA-2025-PF

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Coordinator

VIB VZW
Net EU contribution

Net EU financial contribution. The sum of money that the participant receives, deducted by the EU contribution to its linked third party. It considers the distribution of the EU financial contribution between direct beneficiaries of the project and other types of participants, like third-party participants.

€ 216 240,00
Address
SUZANNE TASSIERSTRAAT 1
9052 ZWIJNAARDE - GENT
Belgium

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Region
Vlaams Gewest Prov. Oost-Vlaanderen Arr. Gent
Activity type
Research Organisations
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Total cost

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