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TNF-α and Microglial Hormetic Involvement in Neurological Health & Migraine

机译：TNF-α和小胶质激素参与神经健康和偏头痛

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Environmental enrichment, i.e., increased intellectual, social, and physical activity makes brain more resilient to subsequent neurological disease. The mechanisms for this effect remain incompletely defined, but evidence shows tumor necrosis factor-alpha (TNF-α) is involved. TNF-α, at acutely high levels, possesses the intrinsic capacity to enhance injury associated with neurological disease. Conversely, the effect of TNF-α at low-levels is nutritive over time, consistent with physiological conditioning hormesis. Evidence shows that neural activity triggers low-level pro-inflammatory signaling involving TNF-α. This low-level TNF-α signaling alters gene expression, resulting in an enhanced resilience to disease. Brain-immune signaling may become maladaptive when increased activity is chronic without sufficient periods of reduced activity necessary for nutritive adaptation. Such tonically increased activity may explain, for example, the transformation of episodic to chronic migraine with related increased susceptibility to spreading depression, the most likely underlying cause of this malady. Thus, TNF-α, whose function is to alter gene expression, and its principal cellular source, microglia, seem powerfully positioned to orchestrate hormetic immune signaling that establishes the phenotype of neurological health and disease from brain activity.
机译：环境的丰富，即智力，社交和体育活动的增加，使大脑对以后的神经系统疾病更具抵抗力。这种作用的机制仍未完全确定，但证据表明涉及肿瘤坏死因子-α（TNF-α）。 TNF-α含量极高，具有增强与神经系统疾病相关的损伤的内在能力。相反，随着时间的流逝，低水平的TNF-α会产生营养，这与生理调节作用有关。有证据表明，神经活动会触发涉及TNF-α的低水平促炎信号传导。这种低水平的TNF-α信号传导会改变基因表达，从而增强对疾病的抵抗力。当活动持续增加，而营养适应所必需的活动减少时间不足时，脑免疫信号可能会适应不良。这种活动性的增加可能解释了例如发作性向慢性偏头痛的转变，同时伴随着对扩散性抑郁症（这可能是该疾病最可能的原因）的敏感性增加。因此，其功能是改变基因表达的TNF-α及其主要的细胞来源小胶质细胞，似乎可以强有力地定位到通过大脑活动建立神经健康和疾病表型的激素性免疫信号传导中。

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