Aging is a key factor in Alzheimer's disease, but it's correlation with the pathology and pathological factors like amyloid-beta remains unclear;	In our study we aimed to provide an extensive characterisation of age-related changes in the gene expression profile of APP23 mice and controls and correlate these changes to pathological and symptomatic features of the model;	We found a clear biphasic expression profile with a developmental and aging phase. The second phase, particularly, displays aging features and similarties with the progression of Alzheimer pathology in human patients;	Processes involved in microglial activation, lysosomal processing, neuronal differantion and cytoskeletal regulation appear key factors in this stage.;	Interestingly, the changes in the gene expression profile of APP23 mice also seem to occur in control animals, but at a later age. The changes appear accelerated and/or exacerbated in APP23 mice. SOURCE: Peter Paul De Deyn University of Antwerp

Pluto Bioinformatics

GSE80465: Aging, microglia and cytoskeletal regulation are key factors in the pathological evolution of the APP23 mouse model for Alzheimers disease