Calcium dysregulation and neuroinflammation: discrete and integrated mechanisms for age-related synaptic dysfunction
作者： Diana M. Sama , Christopher M. Norris
DOI: 10.1016/J.ARR.2013.05.008
关键词: Neuroinflammation 、 Tumor necrosis factor alpha 、 Synapse 、 Long-term potentiation 、 Long-Term Synaptic Depression 、 Cognitive decline 、 Neuroscience 、 Synaptic fatigue 、 Biology 、 Calcineurin
摘要: Some of the best biomarkers age-related cognitive decline are closely linked to synaptic function and plasticity. This review highlights several alterations as they relate Ca2+ dyshomeostasis, through elevation intracellular Ca2+, neuroinflammation, production pro-inflammatory cytokines including interleukin-1 beta (IL-1β) tumor necrosis factor-alpha (TNF-α). Though distinct in many ways, neuroinflammatory signaling mechanisms exhibit extensive cross-talk bidirectional interactions. For instance, cytokine glial cells is strongly dependent on protein phosphatase calcineurin, which shows elevated activity animal models aging disease. In turn, cytokines, such TNF, can augment expression/activity L-type voltage sensitive channels neurons, leading dysregulation, hyperactive calcineurin activity, depression. Thus, addition discussing unique contributions dyshomeostasis this emphasizes how these processes interact hasten changes.
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