Department of Psychiatry, College of Medicine, The Psychiatric Institute, University of Illinois at Chicago, Chicago, IL, USA.
Adv Exp Med Biol. 2023;1411:513-535. doi: 10.1007/978-981-19-7376-5_22.
Peroxisome proliferator-activated receptors (PPARs) are nonsteroid nuclear receptors and transcription factors that regulate several neuroinflammatory and metabolic processes, recently involved in several neuropsychiatric conditions, including Alzheimer's disease, Parkinson's disease, major depressive disorder, post-traumatic stress disorder (PTSD), schizophrenia spectrum disorders, and autism spectrum disorders. PPARs are ligand-activated receptors that, following stimulation, induce neuroprotective effects by decreasing neuroinflammatory processes through inhibition of the nuclear factor kappa-light-chain-enhancer of activated B cell (NF-κB) expression and consequent suppression of pro-inflammatory cytokine production. PPARs heterodimerize with the retinoid X-receptor (RXR) and bind to PPAR-responsive regulatory elements (PPRE) in the promoter region of target genes involved in lipid metabolism, synthesis of cholesterol, catabolism of amino acids, and inflammation. Interestingly, PPARs are considered functionally part of the extended endocannabinoid (eCB) system that includes the classic eCB, anandamide, which act at cannabinoid receptor types 1 (CB1) and 2 (CB2) and are implicated in the pathophysiology of stress-related neuropsychiatric disorders. In preclinical studies, PPAR stimulation improves anxiety and depression-like behaviors by enhancing neurosteroid biosynthesis. The peculiar functional role of PPARs by exerting anti-inflammatory and neuroprotective effects and their expression localization in neurons and glial cells of corticolimbic circuits make them particularly interesting as novel therapeutic targets for several neuropsychiatric disorders characterized by underlying neuroinflammatory/neurodegenerative mechanisms. Herein, we discuss the pathological hallmarks of neuropsychiatric conditions associated with neuroinflammation, as well as the pivotal role of PPARs with a special emphasis on the subtype alpha (PPAR-α) as a suitable molecular target for therapeutic interventions.
过氧化物酶体增殖物激活受体 (PPARs) 是非甾体核受体和转录因子,可调节多种神经炎症和代谢过程,最近涉及多种神经精神疾病,包括阿尔茨海默病、帕金森病、重度抑郁症、创伤后应激障碍 (PTSD) 、精神分裂症谱系障碍和自闭症谱系障碍。PPARs 是配体激活的受体,在受到刺激后,通过抑制核因子 κB(NF-κB)的表达并随后抑制促炎细胞因子的产生,减少神经炎症过程,从而诱导神经保护作用。PPARs 与视黄酸 X 受体 (RXR) 异二聚化,并与涉及脂质代谢、胆固醇合成、氨基酸分解代谢和炎症的靶基因启动子区域中的 PPAR 反应性调节元件 (PPRE) 结合。有趣的是,PPARs 被认为是扩展内源性大麻素 (eCB) 系统的功能部分,该系统包括经典 eCB,即花生四烯酸乙醇胺,其作用于大麻素受体 1 (CB1) 和 2 (CB2),并与应激相关的神经精神疾病的病理生理学有关。在临床前研究中,通过增强神经甾体生物合成,PPAR 刺激可改善焦虑和抑郁样行为。PPARs 通过发挥抗炎和神经保护作用及其在皮质边缘回路神经元和神经胶质细胞中的表达定位,具有独特的功能作用,使其成为几种以潜在神经炎症/神经退行性机制为特征的神经精神疾病的新型治疗靶点。在此,我们讨论了与神经炎症相关的神经精神疾病的病理特征,以及 PPARs 的关键作用,特别强调了亚型 α (PPAR-α) 作为治疗干预的合适分子靶点。