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- W2551116926 abstract "Aging is the key risk factor for Alzheimer's disease (AD). In addition, the amyloid-beta (Aβ) peptide is considered a critical neurotoxic agent in AD pathology. However, the connection between these factors is unclear. We aimed to provide an extensive characterization of the gene expression profiles of the amyloidosis APP23 model for AD and control mice and to evaluate the effect of aging on these profiles. We also correlated our findings to changes in soluble Aβ-levels and other pathological and symptomatic features of the model. We observed a clear biphasic expression profile. The first phase displayed a maturation profile, which resembled features found in young carriers of familial AD mutations. The second phase reflected aging processes and showed similarities to the progression of human AD pathology. During this phase, the model displayed a clear upregulation of microglial activation and lysosomal pathways and downregulation of neuron differentiation and axon guidance pathways. Interestingly, the changes in expression were all correlated to aging in general, but appeared more extensive/accelerated in APP23 mice." @default.
- W2551116926 created "2016-11-30" @default.
- W2551116926 creator A5001850274 @default.
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- W2551116926 creator A5039953079 @default.
- W2551116926 creator A5048208904 @default.
- W2551116926 creator A5060555084 @default.
- W2551116926 creator A5085665229 @default.
- W2551116926 date "2017-02-01" @default.
- W2551116926 modified "2023-09-27" @default.
- W2551116926 title "Aging, microglia and cytoskeletal regulation are key factors in the pathological evolution of the APP23 mouse model for Alzheimer's disease" @default.
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