Amie L. Phinney

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: Investigating the relationship between beta-amyloid deposition and microglia activation in APP23 transgenic mice demonstrated that neuron-derived betaPP is sufficient to induce not only amyloid plaque formation but alsoAmyloid-associated microglial activation similar to that reported in AD, consistent with the idea that microglian activation may be important for the amyloids-associated neuron loss previously reported in these mice.

TL;DR: It is demonstrated that C57BL/6J mice do not exhibit major age-related deficits in spatial learning or hippocampal structure, providing a baseline for further study of mouse brain aging.

TL;DR: Cerebral amyloid deposition has neurotropic effects and is the main cause of aberrant sprouting in AD brain; the magnitude and significance of sprouted in AD have been underestimated; and cerebral amyloids leads to the disruption of neuronal connectivity which, in turn, may significantly contribute to AD dementia.