Michael Willem

This study identifies AETA peptide as a novel contributor to synaptic dysfunction in Alzheimer's disease, particularly in females, through post-mortem analysis and a mouse model.

This study shows that long-term anti-Aβ treatment reduces amyloid plaques and microglial activation but leaves residual plaques with persistent immune activity.

This study identifies iRhom2 as a modifier of ADAM17-mediated TREM2 proteolysis in microglia, linking it to Alzheimer's disease risk.

This study shows that TREM2 deficiency rescues synaptic integration and functional maturation of transplanted neurons in an inflammatory environment.

This study shows that ageing-related myelin dysfunction drives amyloid-beta deposition in Alzheimer's disease mouse models, suggesting myelin integrity as an upstream risk factor.

This study identifies APP's role in regulating NMDAR function during development and aging, showing distinct mechanisms in postnatal and aged stages.

This study shows that chronic PPARγ agonist treatment increases amyloid-beta fibrillarity but improves cognition and synaptic density in mouse models.

This study shows that pre-therapeutic microglia activation and sex predict the response to chronic immunomodulation in AD mouse models using TSPO-PET.

This study identifies proteomic changes in microglia during Alzheimer's disease progression in mouse models, showing fibrillar Aβ drives microglial dysfunction.