Mathieu Bourdenx

Scalable human neuronal models of tauopathy producing endogenous seed-competent 4R tau

This paper develops a scalable human neuronal model of 4R tauopathy with endogenous seed-competent tau for drug discovery.

Trustworthy agentic genomics through versioned skill libraries

This paper shows that trustworthy agentic genome interpretation requires executing validated skills as code rather than relying on models to reason or retrieve information, ensuring deterministic and auditable results.

Spatially resolved transcriptomic identification of thousands of neurons recorded in vivo.

This paper introduces coppaFISH 3D and CASTalign to enable transcriptomic identification of thousands of in vivo recorded neurons at scale.

Spatial Single-Cell Proteomics Reveals Molecular Trajectories Of Tangle-Bearing Neurons In Alzheimer's Disease

The paper uses spatial single-cell proteomics to analyze tangle-bearing neurons in Alzheimer's disease, revealing a continuum of proteomic changes associated with tau pathology.

Distinct mechanistic pathways of early tauopathy revealed by MAPT mutations

This study uses mouse models with tau mutations to show two distinct pathogenic mechanisms in tauopathies, with different progression patterns and responses to amyloid.

Selective suppression of oligodendrocyte-derived amyloid beta rescues neuronal dysfunction in Alzheimer's Disease

This study shows that oligodendrocytes produce amyloid beta in Alzheimer's Disease and that suppressing this production improves brain pathology and neuronal function.

CB1 receptor-mediated inhibitory LTD triggers presynaptic remodeling via protein synthesis and ubiquitination

This study shows that CB1 receptor-mediated inhibitory LTD involves protein synthesis and ubiquitination to cause presynaptic structural changes that reduce GABA release.

Identification of distinct pathological signatures induced by patient-derived α-synuclein structures in non-human primates

The paper uses machine learning to identify neurodegeneration signatures in non-human primates caused by patient-derived α-synuclein structures, showing that small aggregates are as toxic as larger fibrils.