Devrim Kilinc

This paper develops a microfluidic co-culture model to study microglial synapse phagocytosis in AD, finding that APP microglia show enhanced synaptic uptake under inflammation.

This study shows that BIN1 isoform 1 expression in the presynaptic compartment causes synaptotoxicity, leading to synaptic loss and structural changes in Drosophila and rat models.

This paper presents the crystal structure of an APP/talin complex, proposing APP processing as a mechanical signalling pathway involved in synaptic homeostasis and suggesting a new hypothesis for Alzheimer's disease.

This study shows that PLCG2 downregulation impairs synaptic function and increases Alzheimer's disease-related markers in neurons.

This study shows BIN1 regulates L-type calcium channels in neurons, affecting calcium homeostasis and electrical activity, and links these changes to Alzheimer's disease pathology.

The paper identifies FERMT2 as a key modulator of axon guidance and synaptic plasticity in an APP-dependent manner, linking its genetic risk variant to Alzheimer's disease through miRNA regulation.

The paper develops a microfluidic co-culture model to study Aβ1-42-induced synaptotoxicity and shows Pyk2 overexpression in postsynaptic neurons protects against it.

This study shows BIN1 overexpression rescues long-term memory deficits in Tau-overexpressing mice and identifies Thr348 phosphorylation as a key regulator of BIN1-Tau interaction.