Aging, microglia and cytoskeletal regulation are key factors in the pathological evolution of the APP23 mouse model for Alzheimer's disease

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• 作者：Leen Janssen^a ; Marissa L. Dubbelaar^b ; Inge R. Holtman^b ; Jelkje de Boer-Bergsma^c ; Bart J.L. Eggen^b ; Hendrikus W.G.M. Boddeke^b ; Peter P. De Deyn^a ; ^d ; ^e ; ^f ; Debby Van Dam^a ; ^d ; ^{debby.vandam@uantwerpen.be}
• 关键词：Alzheimer's disease ; Gene expression ; RNA sequencing ; Amyloid ; APP23 mouse model ; Inflammation
• 刊名：Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
• 出版年：2017
• 出版时间：February 2017
• 年：2017
• 卷：1863
• 期：2
• 页码：395-405
• 全文大小：1038 K
• 卷排序：1863

文摘

We uncovered two clear phases in the life of APP23 mice: developmental and aging. Development displays similarities to young carriers of familial AD mutations. All gene expression differences between APP23 and control mice correlate with aging. Age-related expression changes appear exacerbated/accelerated in APP23 mice. Microglia and actin cytoskeletal regulation may play a central role in AD pathology.