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针对衰老犬模型中β淀粉样蛋白发病机制的治疗干预。

Therapeutic interventions targeting Beta amyloid pathogenesis in an aging dog model.

机构信息

Sanders Brown Center on Aging, University of Kentucky, Lexington KY, USA.

出版信息

Curr Neuropharmacol. 2011 Dec;9(4):651-61. doi: 10.2174/157015911798376217.

DOI:10.2174/157015911798376217
PMID:22654723
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3263459/
Abstract

Aged dogs and humans share complex cognitive and pathological responses to aging. Specifically, dogs develop Alzheimer's Disease (AD) like beta-amyloid (Aβ) that are associated with cognitive deficits. Currently, therapeutic approaches to prevent AD are targeted towards reduced production, aggregation and increased clearance of Aβ. The current review discusses cognition and neuropathology of the aging canine model and how it has and continues to be useful in further understanding the safety and efficacy of potential AD prevention therapies targeting Aβ.

摘要

老年犬和人类在衰老方面具有复杂的认知和病理反应。具体来说,狗会出现类似于阿尔茨海默病(AD)的β-淀粉样蛋白(Aβ),这与认知缺陷有关。目前,预防 AD 的治疗方法主要针对减少 Aβ的产生、聚集和增加其清除。本文综述了衰老犬模型的认知和神经病理学,以及它在进一步理解针对 Aβ的潜在 AD 预防治疗的安全性和疗效方面的作用和持续作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54b3/3263459/dbee90e639d8/CN-9-651_F2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54b3/3263459/d9804e54f4be/CN-9-651_F1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54b3/3263459/dbee90e639d8/CN-9-651_F2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54b3/3263459/d9804e54f4be/CN-9-651_F1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/54b3/3263459/dbee90e639d8/CN-9-651_F2.jpg

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本文引用的文献

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Decreased clearance of CNS beta-amyloid in Alzheimer's disease.阿尔茨海默病患者中枢神经系统β-淀粉样蛋白清除减少。
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Aβ aggregation profiles and shifts in APP processing favor amyloidogenesis in canines.Aβ 聚集谱和 APP 加工的改变有利于犬类的淀粉样蛋白形成。
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