Tizabi Yousef, Antonelli Marta C, Tizabi Daniela, Aschner Michael
Department of Pharmacology, Howard University College of Medicine, Washington, DC, USA.
Facultad de Medicina, UBA, Instituto de Biología Celular y Neurociencia "Prof. E. De Robertis", Buenos Aires, Argentina.
Neurochem Res. 2025 Jan 27;50(2):85. doi: 10.1007/s11064-025-04336-8.
The specific pathogeneses of schizophrenia (SCZ) remain an enigma despite extensive research that has implicated both genetic and environmental factors. Recent revelations that dysregulated immune system caused by glial cell overactivation result in neuroinflammation, a key player in neurodegenerative as well as neuropsychiatric disorders including SCZ are providing novel clues on potential therapeutic interventions. Here, we review the roles of glial cells (Dr. Arne Schousboe's passion) and two of their most implicated receptors, toll-like receptors (TLRs), and nicotinic cholinergic receptors, in SCZ pathology with suggestions as potential targets in this devastating neuropsychiatric condition.
尽管进行了大量研究,涉及到遗传和环境因素,但精神分裂症(SCZ)的具体发病机制仍然是个谜。最近有研究表明,神经胶质细胞过度激活导致免疫系统失调,进而引发神经炎症,而神经炎症是神经退行性疾病以及包括SCZ在内的神经精神疾病的关键因素,这为潜在的治疗干预提供了新线索。在此,我们综述了神经胶质细胞(阿恩·舒斯博博士的研究重点)及其最相关的两种受体——Toll样受体(TLRs)和烟碱型胆碱能受体在SCZ病理中的作用,并提出将其作为这种毁灭性神经精神疾病潜在治疗靶点的建议。