Gomez-Pinilla F, Myers Sydney K
Department of Integrative Biology and Physiology, University of California, Los Angeles, CA 90095, USA; Department of Neurosurgery, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA.
Department of Neurosurgery, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA.
Prog Neurobiol. 2025 Apr;247:102733. doi: 10.1016/j.pneurobio.2025.102733. Epub 2025 Mar 1.
Traumatic brain injury (TBI) is a major cause of death and disability worldwide. Most current treatments for TBI and other neurological disorders focus on the brain, often overlooking the significant contributions of peripheral organs to disease progression. Emerging evidence suggests that organs such as the liver and adipose tissue play crucial roles in TBI pathogenesis. The liver synthesizes lipids and proteins vital for brain function, while adipose tissue provides hormones and metabolites that influence brain activity. New research indicates that the liver and adipose tissue work in concert with the hypothalamus to regulate essential processes, such as body temperature, which become disrupted in TBI. Additionally, the brain-peripheral axis-a complex network of visceral nerve pathways, hormones, and metabolites-plays a bidirectional role in regulating brain plasticity and function. Understanding how TBI leads to dysregulation of the liver, adipose tissue, and other organs could unlock new therapeutic opportunities for treating TBI and related neurological disorders. The intricate autonomic network involving hypothalamic and enteric neurons, along with visceral nerve pathways and hormones, presents both pathological targets and therapeutic potential. We examine scientific evidence suggesting that correcting disturbances in systemic physiology could enhance the brain's capacity for healing. However, the interdependence of this autonomic network implies that treating dysfunction in one area may affect others. Therefore, we also explore the mechanisms by which diet and exercise can comprehensively impact the brain-peripheral axis, supporting the healing process. CHEMICAL COMPOUNDS: D-Fructose (PubChem CID 2723872); docosahexaenoic acid (PubChem CID 45934466); eicosapentaenoic acid (PubChem 5282847).
创伤性脑损伤（TBI）是全球范围内死亡和残疾的主要原因。目前大多数针对TBI和其他神经系统疾病的治疗都集中在大脑，常常忽视外周器官对疾病进展的重大影响。新出现的证据表明，肝脏和脂肪组织等器官在TBI发病机制中起着关键作用。肝脏合成对脑功能至关重要的脂质和蛋白质，而脂肪组织则提供影响脑活动的激素和代谢物。新的研究表明，肝脏和脂肪组织与下丘脑协同作用，调节体温等基本生理过程，而这些过程在TBI中会受到破坏。此外，脑-外周轴——一个由内脏神经通路、激素和代谢物组成的复杂网络——在调节脑可塑性和功能方面发挥着双向作用。了解TBI如何导致肝脏、脂肪组织和其他器官的调节失调，可能为治疗TBI和相关神经系统疾病带来新的治疗机会。涉及下丘脑和肠神经元的复杂自主神经网络，连同内脏神经通路和激素，既呈现出病理靶点，也具有治疗潜力。我们研究了科学证据，表明纠正全身生理紊乱可以增强大脑的愈合能力。然而，这个自主神经网络的相互依存性意味着治疗一个区域的功能障碍可能会影响其他区域。因此，我们还探讨了饮食和运动能够全面影响脑-外周轴、支持愈合过程的机制。化学化合物：D-果糖（PubChem CID 2723872）；二十二碳六烯酸（PubChem CID 45934466）；二十碳五烯酸（PubChem 5282847）。
