Julien Chapuis

The Alzheimer's disease-associated rs28834970 variant in PTK2B impairs electrical activity and regulates Tau phosphorylation and APP processing in human neuronal cultures

This study identifies the rs28834970 variant in PTK2B as a risk factor for Alzheimer's disease, showing it impairs PYK2 function, increases Tau phosphorylation, and alters APP processing in human neuronal cultures.

Inflammation-enhanced synapse-specific phagocytosis by adult APP microglia in a microfluidic neuron-microglia co-culture model

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.

The structure of an Amyloid Precursor Protein/talin complex indicates a mechanical basis of Alzheimer's Disease.

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.

Non-microglial downregulation of PLCG2 impairs synaptic function and elicits Alzheimer disease-related hallmarks

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

The Alzheimer susceptibility gene BIN1 induces isoform-dependent neurotoxicity through early endosome defects

This study shows that BIN1 isoform1 causes early endosome defects and neurodegeneration in Drosophila and human neurons, linking it to Alzheimer's disease pathology.

Alzheimer's genetic risk factor FERMT2 (Kindlin-2) controls axonal growth and synaptic plasticity in an APP-dependent manner.

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.

Pyk2 Overexpression in Postsynaptic Neurons Blocks Aβ1-42-induced Synaptotoxicity in a Microfluidic Co-Culture Model

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

BIN1 recovers tauopathy-induced long-term memory deficits in mice and interacts with Tau through Thr348 phosphorylation

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.