Karl-Heinz Wiederhold

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 suggested that a redistribution of synaptic drive between silent and hyperactive neurons, rather than an overall decrease in synaptic activity, provides a mechanism for the disturbed cortical function in Alzheimer's disease.

TL;DR: Thy1 transgene expression of wild-type human α-synuclein resulted in similar pathological changes, thus supporting a central role for mutant and wild- type α- Synuclein in familial and idiotypic forms of diseases with neuronal α- synucleinopathy and Lewy pathology.

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.