帕金森病(PD)是一种常见的神经元变性疾病,主要症状是震颤,姿势和肌张力障碍及运动减少;典型病理表现为黑质致密带神经元的缺失,镜下可见部分细胞内出现嗜伊红包涵体(Lewy小体)。随着医学分子生物学的进展,人们普遍认为其致病基因在PD的发病过程中居于主导地位。目前已经定PD的致病基因位点有12个(4q21-23,2p13,4p14-16,3/4p15,4p14/4p14-15,12p11-q13,6q25-27,1p35-36,1p36,1p32,1q36-37,xq21-25)。本研究主要阐述上述基因位点改变后的相关基因的功能研究进展。 Parkinson’s disease (PD) is a common neurodegenerative disease, the main symptoms are tremor, postural and dystonia and motor loss; typical pathology showed the loss of substantia nigra neurons, microscopic appearance of some cells Eosinophil inclusions (Lewy bodies). With the progress of medical molecular biology, it is generally considered that the causative gene plays a dominant role in the pathogenesis of PD. At present, there are 12 pathogenic sites of PD (4q21-23,2p13,4p14-16,3 / 4p15,4p14 / 4p14-15,12p11-q13,6q25-27,1p35-36,1p36,1p32, 1q36-37, xq21-25). This research mainly expounds the research progress of the function of related genes after the above gene loci are changed.