Galectin 3:A new player in the pathogenesis of Parkinson's disease
Juan García-Revilla1
Jose Luis Venero2
José A.Rodríguez-Gómez2
1.Experimental Neuroinflammation Laboratory,Department of Experimental Medical Science,Lund University,Lund,Sweden;Instituto de Biomedicina de Sevilla,IBiS/Hospital Universitario Virgen del Rocío/CSIC/Universidad de Sevilla,Seville,Spain;Departamento de Bioquímica y Biología Molecular,Facultad de Farmacia,Universidad de Sevilla,Seville,Spain2.Instituto de Biomedicina de Sevilla,IBiS/Hospital Universitario Virgen del Rocío/CSIC/Universidad de Sevilla,Seville,Spain;Departamento de Bioquímica y Biología Molecular,Facultad de Farmacia,Universidad de Sevilla,Seville,Spain
摘要：Different forms of programmed cell death have been described to participate in the degeneration of dopaminergic neurons in Parkinson's disease(PD). Given the critical role that disturbance of mitochondrial homeostasis plays in the pathogenesis of PD,apoptosis can be reasonably considered as one of the cell death pathways involved in neuronal loss (Schon and Przedborski,2011). Multiple lines of evidence support that proposal such as the observations in postmortem human brain samples of PD patients including mitochondrial complex I deficiency,reactive oxygen species generation,and oxidative damage to lipids,proteins,and DNA,among others. Active forms of caspase-8,-9 and-3,the ultimate executor apoptotic caspase,have also been detected in nigrostriatal dopaminergic neurons in the brains of PD patients. Therefore,a relevant question in the field is whether the blockage of the apoptotic pathway would be able to prevent cell death and become a therapeutical option for this disease.
机标关键词：galectinparkinsonplayerdiseasepathogenesis
论文发表日期：2026-03-30
在线出版日期：2026-03-18（本平台首次上网日期，不代表文献的发表时间）
页数：2( 1132-1133 )