Álvarez-Luquín Diana D, González-Fernández Rubén R, Torres-Velasco Martin E, Ichikawa-Escamilla Eduardo, Arce-Sillas Asiel, Martínez-Martínez Eduardo, Miranda-Narvaez Clara L, Rodríguez-Ramírez Juan F, Adalid-Peralta Laura
Laboratorio de Reprogramación Celular del Instituto de Fisiología Celular, UNAM, en el Instituto Nacional de Neurología y Neurocirugía "Manuel Velasco Suarez", Insurgentes Sur 3877, La Fama, Tlalpan, Ciudad de Mexico, 14269, México.
Departamento de Investigación en Virología y Micología, Instituto Nacional de Enfermedades Respiratorias "Ismael Cosío Villegas", Calzada de Tlalpan 4502, Sección XVI, Tlalpan, Ciudad de Mexico, 14080, México.
Behav Brain Funct. 2025 May 31;21(1):14. doi: 10.1186/s12993-025-00279-w.
Parkinson's disease (PD) is a progressive neurodegenerative disorder that affects dopaminergic neurons in the substantia nigra pars compacta. It is a complex disease that is strongly influenced by environmental and genetic factors. While the exact causes of PD are not well understood, research on the effects of toxic substances that induce neuronal death has shed some light on the etiology of the disease. In addition, studies have implicated protein aggregation and impaired mitochondrial, endoplasmic reticulum (ER), proteasome, and/or lysosomal function in the pathogenesis of PD. This review focuses on the alterations in intraneuronal organelles and the role of toxic agents that lead to organelle damage and neurodegeneration that characterize PD. We describe in vivo and in vitro models that have been used to elucidate the factors that lead to the death of dopaminergic neurons and summarize the molecular mechanisms that may underlie the changes that promote neurodegeneration. A deeper understanding of the mechanisms of neuronal death may help us to develop new therapies and interventions to delay or prevent the progression of PD.
帕金森病(PD)是一种进行性神经退行性疾病,会影响黑质致密部的多巴胺能神经元。它是一种复杂的疾病,受到环境和遗传因素的强烈影响。虽然PD的确切病因尚不完全清楚,但对诱导神经元死亡的有毒物质的影响的研究为该疾病的病因提供了一些线索。此外,研究表明蛋白质聚集以及线粒体、内质网(ER)、蛋白酶体和/或溶酶体功能受损与PD的发病机制有关。本综述重点关注神经元内细胞器的改变以及导致细胞器损伤和神经退行性变的有毒物质的作用,这些特征是PD的典型表现。我们描述了用于阐明导致多巴胺能神经元死亡的因素的体内和体外模型,并总结了可能促进神经退行性变的变化背后的分子机制。对神经元死亡机制的更深入理解可能有助于我们开发新的治疗方法和干预措施,以延缓或预防PD的进展。