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用于研究记忆及胰岛素在大脑中作用的SAMP8小鼠。

The SAMP8 mouse for investigating memory and the role of insulin in the brain.

作者信息

Rhea Elizabeth M, Banks William A

机构信息

Division of Gerontology and Geriatric Medicine, Department of Medicine, University of Washington School of Medicine, United States.

Division of Gerontology and Geriatric Medicine, Department of Medicine, University of Washington School of Medicine, United States.

出版信息

Exp Gerontol. 2017 Aug;94:64-68. doi: 10.1016/j.exger.2016.12.009. Epub 2016 Dec 12.

DOI:10.1016/j.exger.2016.12.009
PMID:27979769
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5468519/
Abstract

SAMP8 mice exhibit changes that commonly occur with normal aging late in life, but do so at a much earlier age. These changes include impairments in learning and memory as early as 8months of age and so the SAMP8 is a useful model to investigate those age-related brain changes that may affect cognition. As brain insulin signaling and memory decline with aging, the SAMP8 model is useful for investigating these changes and interventions that might prevent the decline. This review will summarize the SAMP8 mouse model, highlight changes in brain insulin signaling and its role in memory, and discuss intranasal insulin delivery in investigating effects on insulin metabolism and memory in the SAMP8 mice.

摘要

SAMP8小鼠表现出通常在正常衰老后期出现的变化,但在更早的年龄就会出现。这些变化包括早在8个月大时学习和记忆就出现损伤,因此SAMP8是研究那些可能影响认知的与年龄相关的大脑变化的有用模型。随着大脑胰岛素信号传导和记忆力随着年龄增长而下降,SAMP8模型对于研究这些变化以及可能预防这种下降的干预措施很有用。本综述将总结SAMP8小鼠模型,强调大脑胰岛素信号传导的变化及其在记忆中的作用,并讨论鼻内胰岛素给药对SAMP8小鼠胰岛素代谢和记忆的影响。

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Antisense against Amyloid-β Protein Precursor Reverses Memory Deficits and Alters Gene Expression in Neurotropic and Insulin-Signaling Pathways in SAMP8 Mice.针对淀粉样β蛋白前体的反义核酸可逆转SAMP8小鼠的记忆缺陷并改变神经营养和胰岛素信号通路中的基因表达。
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