Raghavan Cibin T
Department of Biochemistry, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Thiruvananthapuram, 695 011, Kerala, India.
Molecular Genetics Unit, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Thiruvananthapuram, 695 011, Kerala, India.
J Mol Neurosci. 2024 Dec 10;74(4):114. doi: 10.1007/s12031-024-02297-1.
Advanced glycation end products (AGEs) have attracted interest as therapeutic targets for neurodegenerative diseases. AGEs facilitate the onset and progression of various neurogenerative disorders due to their ability to promote cross-linking and aggregation of proteins. Further, the interaction between AGEs and receptor for AGEs (RAGE) activates neuroinflammatory, oxidative stress and excitotoxicity processes that contribute to neuronal cell death. Various therapeutic efforts have targeted lowering the production of AGEs, inhibiting RAGE or inhibiting some of the processes of the AGE-RAGE axis as potential treatments for these disorders. Whereas effective treatments for many neurodegenerative disorders remain elusive, such efforts offer promise to slow the progression of diseases such as Alzheimer's disease (AD), Parkinson's disease (PD) and Huntington's disease (HD).
晚期糖基化终末产物（AGEs）作为神经退行性疾病的治疗靶点已引起关注。AGEs由于能够促进蛋白质的交联和聚集，从而促进各种神经退行性疾病的发生和发展。此外，AGEs与AGEs受体（RAGE）之间的相互作用激活了神经炎症、氧化应激和兴奋性毒性过程，这些过程导致神经元细胞死亡。各种治疗措施旨在降低AGEs的产生、抑制RAGE或抑制AGE-RAGE轴的某些过程，作为这些疾病的潜在治疗方法。尽管许多神经退行性疾病的有效治疗方法仍然难以捉摸，但这些努力有望减缓阿尔茨海默病（AD）、帕金森病（PD）和亨廷顿舞蹈病（HD）等疾病的进展。
