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通过 Abl 激酶抑制实现帕金森病修饰:一个机会。

Parkinson's Disease Modification Through Abl Kinase Inhibition: An Opportunity.

机构信息

Inhibikase Therapeutics, Inc., Atlanta, Georgia, USA.

Department of Neurology and Department of Neuroscience, Mount Sinai School of Medicine, New York, New York, USA.

出版信息

Mov Disord. 2022 Jan;37(1):6-15. doi: 10.1002/mds.28858. Epub 2021 Nov 23.

Abstract

Parkinson's disease (PD) is the second most prevalent neurodegenerative disease of the central nervous system, with an estimated 5 000 000 cases worldwide. Historically characterized by the progressive loss of dopaminergic neurons in the substantia nigra pars compacta, PD pathology is now known to be widespread and to affect serotonin, cholinergic and norepinephrine neurons as well as nerve cells in the olfactory system, cerebral hemisphere, brain stem, spinal cord, and peripheral autonomic nervous system. PD pathology is characterized by the accumulation of misfolded α-synuclein, which is thought to play a critical role in the etiopathogenesis of the disease. Animal models of PD suggest that activation of the Abelson tyrosine kinase (c-Abl) plays an essential role in the initiation and progression of α-synuclein pathology and neurodegeneration. These studies demonstrate that internalization of misfolded α-synuclein activates c-Abl, which phosphorylates α-synuclein and promotes α-synuclein pathology within the affected neurons. Additionally, c-Abl inactivates parkin, disrupting mitochondrial quality control and biogenesis, promoting neurodegeneration. Post-mortem studies of PD patients demonstrate increased levels of tyrosine phosphorylated α-synuclein, consistent with the activation of c-Abl in human disease. Although the c-Abl inhibitor nilotinib failed to demonstrate clinical benefit in two double-blind trials, novel c-Abl inhibitors have been developed that accumulate in the brain and may inhibit c-Abl at saturating levels. These novel inhibitors have demonstrated benefits in animal models of PD and have now entered clinical development. Here, we review the role of c-Abl in the neurodegenerative disease process and consider the translational potential of c-Abl inhibitors from model studies to disease-modifying therapies for Parkinson's disease. © 2021 Inhibikase Therapeutics, Inc. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson Movement Disorder Society.

摘要

帕金森病(PD)是中枢神经系统第二大常见的神经退行性疾病,全球估计有 500 万例。PD 病史以黑质致密部多巴胺能神经元进行性丧失为特征,目前已知其病理学广泛存在,并影响 5-羟色胺、胆碱能和去甲肾上腺素能神经元以及嗅觉系统、大脑半球、脑干、脊髓和外周自主神经系统的神经细胞。PD 病理学的特征是错误折叠的 α-突触核蛋白的积累,据认为这在疾病的病因发病机制中起关键作用。PD 的动物模型表明,Abelson 酪氨酸激酶(c-Abl)的激活在 α-突触核蛋白病理学和神经退行性变的起始和进展中发挥重要作用。这些研究表明,错误折叠的 α-突触核蛋白的内化激活了 c-Abl,c-Abl 使 α-突触核蛋白磷酸化,并促进受影响神经元中的 α-突触核蛋白病理学。此外,c-Abl 使 parkin 失活,破坏线粒体质量控制和生物发生,促进神经退行性变。PD 患者的死后研究表明,酪氨酸磷酸化的 α-突触核蛋白水平升高,与人类疾病中 c-Abl 的激活一致。尽管 c-Abl 抑制剂 nilotinib 在两项双盲试验中未能显示出临床益处,但已开发出新型 c-Abl 抑制剂,这些抑制剂在大脑中积累,并可能以饱和水平抑制 c-Abl。这些新型抑制剂在 PD 的动物模型中显示出益处,现已进入临床开发阶段。在这里,我们回顾了 c-Abl 在神经退行性疾病过程中的作用,并考虑了从模型研究到帕金森病疾病修饰疗法的 c-Abl 抑制剂的转化潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/adda/9544958/a6ebd1401351/MDS-37-6-g002.jpg

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