Early molecular and synaptic dysfunctions in the prodromal stages of Alzheimer's disease: focus on TNF-alpha and IL-1 beta

被引：11

作者：

Cavanagh, Chelsea ^{[1
,2
]}

Colby-Milley, Jessica ^{[1
,2
]}

Farso, Mark ^{[1
,2
]}

Krantic, Slavica ^{[1
,2
]}

Quirion, Remi ^{[1
,2
]}

机构：

[1] McGill Univ, Dept Psychiat, Douglas Mental Hlth Univ Inst, 6875 Boul Lasalle, Verdun, PQ H4H 1R3, Canada

[2] McGill Univ, Montreal, PQ H3A 2T5, Canada

来源：

FUTURE NEUROLOGY | 2011年 / 6卷 / 06期

基金：

加拿大健康研究院;

关键词：

amyloid-beta oligomer; cytokine; hyperexcitability; neuroinflammation; synaptic plasticity;

D O I：

10.2217/FNL.11.50

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

Alterations in cytokine expression as well as deficits in synaptic activity are two features observed in early, prodromal stages of Alzheimer's disease (AD). The cytokines TNF-alpha and IL-1 beta are not only mediators of immune responses, but are also involved in regulating synaptic activity through their effects on neuronal excitability and Hebbian plasticity. We propose that early changes occurring in the AD brain, such as increases in soluble amyloid-b oligomers, may increase the expression of certain cytokines and subsequently cause alterations in cytokinemediated synaptic activity. A shift of focus towards the prodromal stages of AD, which incorporate the earliest detectable molecular, electrophysiological and behavioral alterations, may provide novel therapeutic targets and potential biomarkers for this currently incurable neurodegenerative disease.

引用

页码：757 / 769

页数：13

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