Connectivity of Pathology: The Olfactory System as a Model for Network-Driven Mechanisms of Alzheimer's Disease Pathogenesis

被引：33

作者：

Franks, Katherine H. ^{[1
]}

Chuah, Meng Inn ^{[1
]}

King, Anna E. ^{[1
]}

Vickers, James C. ^{[1
]}

机构：

[1] Univ Tasmania, Fac Hlth, Wicking Dementia Res & Educ Ctr, Hobart, Tas, Australia

来源：

FRONTIERS IN AGING NEUROSCIENCE | 2015年 / 7卷

关键词：

Alzheimer's disease; olfaction; denervation; enrichment; connectivity; amyloid beta; MILD COGNITIVE IMPAIRMENT; ALTERS CELLULAR PHENOTYPES; TRANSGENIC MOUSE MODEL; TRAUMATIC BRAIN-INJURY; AMYLOID-BETA BURDEN; TAU PATHOLOGY; NEURODEGENERATIVE DISEASES; PROTEIN IMMUNOREACTIVITY; BULB; DYSFUNCTION;

D O I：

10.3389/fnagi.2015.00234

中图分类号：

R592 [老年病学]; C [社会科学总论];

学科分类号：

03 ; 0303 ; 100203 ;

摘要：

The pathogenesis of Alzheimer's disease (AD) has been postulated to preferentially impact specific neural networks in the brain. The olfactory system is a well-defined network that has been implicated in early stages of the disease, marked by impairment in olfaction and the presence of pathological hallmarks of the disease, even before clinical presentation. Discovering the cellular mechanisms involved in the connectivity of pathology will provide insight into potential targets for treatment. We review evidence from animal studies on sensory alteration through denervation or enrichment, which supports the notion of using the olfactory system to investigate the implications of connectivity and activity in the spread of pathology in AD.

引用

页数：12

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