Presynaptic Dysfunction by Familial Factors in Parkinson Disease.
- Author:
Wongyoung LEE
1
;
Soulmee KOH
;
Soondo HWANG
;
Sung Hyun KIM
Author Information
- Publication Type:Review
- Keywords: Parkinson disease; Synapse; Synaptic transmission; Synaptic vesicles
- MeSH: Alzheimer Disease; Brain; Neurodegenerative Diseases; Parkinson Disease*; Pars Compacta; Phosphotransferases; Presynaptic Terminals; Synapses; Synaptic Transmission; Synaptic Vesicles
- From:International Neurourology Journal 2018;22(Suppl 3):S115-S121
- CountryRepublic of Korea
- Language:English
- Abstract: Parkinson disease (PD) is the second most prevalent neurodegenerative disorder after Alzheimer disease. The loss of specific brain area, the substantia nigra pars compacta is known as a major etiology, however it is not fully understood how this neurodegeneration is initiated and what precisely causes this disease. As one aspect of pathophysiology for PD, synaptic dysfunction (synaptopathy) is thought to be an earlier appearance for neurodegeneration. In addition, some of the familial factors cumulatively exhibit that these factors such as α-synuclein, leucine-rich repeat kinase 2, parkin, PTEN-induced kinase 1, and DJ-1 are involved in the regulation of synaptic function and missense mutants of familial factors found in PD-patient show dysregulation of synaptic functions. In this review, we have discussed the physiological function of these genetic factors in presynaptic terminal and how dysregulation of presynaptic function by genetic factors might be related to the pathogenesis of Parkinson disease.
