Rudenok M M, Alieva A Kh, Nikolaev M A, Kolacheva A A, Ugryumov M V, Pchelina S N, Slominsky P A, Shadrina M I
Institute of Molecular Genetics, Russian Academy of Sciences, Moscow, 123182 Russia.
St. Petersburg National Research Academic University of the Russian Academy of Sciences, St. Petersburg, 194021 Russia.
Mol Biol (Mosk). 2019 Jan-Feb;53(1):28-36. doi: 10.1134/S0026898419010142.
Parkinson's disease (PD) characterized with slow continuous degeneration of dopaminergic neurons in the substantia nigra is one of the most common neurodegenerative diseases, but its etiology and pathogenesis are not fully understood. The pathogenesis of PD involves the impairment of lysosomal autophagy, which also contributes to lysosomal storage disorders (LSDs). In this work, the expression of genes related to lysosomal autophagy: Hspa8, Lamp2, Tfam, Slc18a2, and Vps35, was analyzed in the brain tissues of mice with the earliest stage of MPTP-induced PD. The detected decrease in Hspa8 and Lamp2 mRNA levels suggests that dysfunction of lysosomal autophagy maybe involved in the earliest stages of PD pathogenesis. A decrease in the rate of lysosomal autophagy may affect the accumulation of damaged proteins and the formation of protein inclusions in PD. Genes related to the lysosome function may be involved in development of both LSD and PD at the earliest stages of these pathophysiological processes.
帕金森病（PD）的特征是黑质中多巴胺能神经元持续缓慢退化，是最常见的神经退行性疾病之一，但其病因和发病机制尚未完全明确。PD的发病机制涉及溶酶体自噬功能受损，这也与溶酶体贮积症（LSDs）有关。在本研究中，分析了MPTP诱导的早期PD小鼠脑组织中与溶酶体自噬相关的基因：Hspa8、Lamp2、Tfam、Slc18a2和Vps35的表达。检测到Hspa8和Lamp2 mRNA水平降低，表明溶酶体自噬功能障碍可能参与了PD发病机制的早期阶段。溶酶体自噬速率降低可能会影响PD中受损蛋白质的积累和蛋白质包涵体的形成。与溶酶体功能相关的基因可能在这些病理生理过程的最早阶段参与LSD和PD的发展。
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