Marie‐Claude Potier

The paper examines how diet and genetic factors affect metabolomics and microbiota in a Down syndrome mouse model, identifying interactions that influence metabolic pathways.

This study evaluates the efficacy of 5IA in the Dp(16)1Yey mouse model of Down syndrome, finding improved motor coordination but no cognitive rescue, suggesting divergent pathophysiology compared to Ts65Dn models.

This study identifies TLR9's role in microglial activation and lysosomal dysfunction in Alzheimer's disease, showing its inhibition reduces pathology and cognitive defects.

This study shows that PSEN1 mutations disrupt regulated intramembrane proteolysis in astrocytes, leading to enhanced inflammatory responses and contributing to familial Alzheimer's disease progression.

The paper examines mitochondrial alterations in fibroblasts from Alzheimer's disease patients and links them to clinical hallmarks and cognitive decline.

The paper introduces a new mouse model, Ts66Yah, for Down syndrome that replicates DS cognitive features and reveals genetic interactions between triplicated regions homologous to Hsa21 and unrelated regions.

The paper establishes the 3D anatomy of meningeal lymphatic vasculature and CSF drainage in mice and humans using imaging techniques, showing conserved lymphatic structures.

The paper examines longitudinal EEG changes in pre-clinical Alzheimer's Disease, finding increased theta-band power in specific brain regions in amyloid-positive individuals.

The paper identifies the molecular signature and connectivity specificity of Martinotti cell inhibitory circuits in the mouse barrel cortex, revealing target-specific synaptic properties and the role of 5-GABAARs in cognitive functions.

This study shows that mutations in the juxtamembrane cholesterol-binding site of APP reduce production of toxic Aβ40 and Aβ42 peptides and increase shorter, less toxic Aβ peptides.

The paper identifies specific inhibitory circuit alterations in the prefrontal cortex of a Down syndrome mouse model, linking them to cognitive dysfunction.

This study shows that Akt phosphorylation of Huntingtin regulates axonal transport of APP and presynaptic levels, affecting synaptic homeostasis and learning.