Remco V. Klaassen

The paper identifies novel interactors of TREML1 and TREML2 using proteomics, highlighting their roles in lipid trafficking and immunity.

The paper compares whole-tissue and synaptosome proteomics using LC-MS/MS to evaluate synaptic protein detection, recommending a tiered approach for studying brain disorders.

The paper shows that NREM sleep oscillations drive synaptic proteome remodelling, promoting stabilization and memory consolidation, while altered oscillations in a disorder lead to synaptic weakening.

This study shows that deleting GFAP and Vimentin in astrocytes reduces early synaptic and cognitive dysfunction in Alzheimer's mice by improving protein synthesis and astrocyte function.

This study shows that SFRP1 overexpression in astrocytes causes synaptic dysfunction and memory impairment in mice, suggesting SFRP1 as a therapeutic target for Alzheimer's disease.

This study shows that β-amyloid oligomers cause synaptic depression by removing GluA3-containing AMPARs from synapses, requiring PDZ protein interaction.

The paper investigates nanoscale synaptic changes during two LTD protocols, showing NMDAR-dependent LTD reorganizes PSD-95 to enhance synaptic facilitation.