Department of Neurology, Juntendo University Graduate School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan.
Research Institute for Diseases of Old Age, Juntendo University Graduate School of Medicine, Tokyo, 113-8421, Japan.
J Neural Transm (Vienna). 2017 Nov;124(11):1395-1400. doi: 10.1007/s00702-017-1779-7. Epub 2017 Sep 11.
Genes encoding lysosomal proteins, such as ATP13A2 and GBA, are associated with familial Parkinson's disease (PD). Heterozygous mutations in GBA are strongly associated with familial PD. ATP13A2, which encodes a lysosomal P-type ATPase, has been identified as the causative gene for Kufor-Rakeb syndrome. While lysosomal dysfunction due to these mutations exhibited early onset Parkinsonism, each animal model demonstrated different pathological mechanisms. Clinicogenetic and animal model studies recently identified several lysosomal alterations that play a role in the pathogenesis of PD.
编码溶酶体蛋白的基因,如 ATP13A2 和 GBA,与家族性帕金森病(PD)有关。GBA 的杂合突变与家族性 PD 强烈相关。ATP13A2 编码溶酶体 P 型 ATP 酶,已被确定为 Kufor-Rakeb 综合征的致病基因。虽然这些突变导致的溶酶体功能障碍表现为早发性帕金森病,但每种动物模型都表现出不同的病理机制。临床遗传学和动物模型研究最近确定了几种溶酶体改变在 PD 的发病机制中起作用。