Pascal Kienlen‐Campard

This study identifies mitochondrial dysfunction as a key feature of brain senescence in telomerase-deficient mice, linking telomere attrition to impaired mitochondrial function and region-specific neuronal vulnerability.

This study shows that the N141I PS2 mutation disrupts lipid homeostasis and mitochondrial dynamics by downregulating Gbf1, suggesting a new amyloid-independent pathway in Alzheimer's disease.

This study maps stage-dependent tau post-translational modifications across Alzheimer's disease progression, revealing early phosphorylation and later ubiquitination events associated with tau aggregation.

The paper identifies Gbp2b as an early biomarker of tauopathy in the olfactory epithelium of PS19 mice through transcriptomic analysis across different ages.

This study shows that pathological tau spreads from the olfactory epithelium to brain regions in AD models and suggests targeting the olfactory epithelium to slow tauopathy progression.

This study investigates the effects of hexameric β-amyloid assemblies on neuronal viability and amyloid deposition, finding no direct toxicity but an aggravating role in amyloid formation.

The paper shows that PS1 and PS2 deficiency in primary neurons and astrocytes does not cause mitochondrial dysfunction, contrasting with findings in immortalized cell lines.

The paper shows that dimeric orientations of C99 influence γ-secretase cleavage lines, affecting Aβ42 processing and gene transcription.

This study identifies NPAS4 as a target of APP regulation, showing APP controls excitatory/inhibitory synaptic inputs by modulating NPAS4 expression in neurons.

This study investigates the roles of endosomal-lysosomal and proteasomal pathways in processing APP-derived fragments, showing distinct degradation mechanisms for full-length APP and overexpressed C99.