Christine Sturchler-Pierrat

TL;DR: These mice resemble major features of AD pathology and suggest a central role of A beta in the pathogenesis of the disease.

TL;DR: It is shown that presenilin-1 forms a complex with β-catenin in vivo that increases β-Catenin stability, which increases neuronal vulnerability to apoptosis induced by amyloid-β protein.

TL;DR: It is reported that these mice exhibit selective neuronal death in the brain regions that are most affected in AD, suggesting that amyloid plaque formation is directly involved in AD neuron loss.

TL;DR: App-null mice on an App-null background developed a similar degree of both plaques and CAA, providing further evidence that a neuronal source of APP/Abeta is sufficient to induce cerebrovascular amyloid and associated neurodegeneration.

TL;DR: This HCHWA-D mouse model is the first to develop robust CAA in the absence of parenchymal amyloid, highlighting the key role of neuronally produced Aβ to vascular amyloids pathology and emphasizing the differing roles of Aβ40 and Aβ42 in vascular and paren chymalAmyloid pathology.