Parkinson's disease (PD) is a progressive neurodegenerative disease caused by 
interaction of genetic and environmental factors. To date, genetic genes and 
variants causing PD remain largely unknown. Autophagy is a conserved cellular 
process including three subtypes, macroautophagy (hereafter referred to as 
autophagy), microautophagy and chaperone-mediated autophagy (CMA). Although 
reduced CMA and induced autophagy are observed in human PD brain samples, cell 
and animal PD models, CMA and autophagy have not been systemically studied in 
sporadic PD patients. In the peripheral leukocytes of sporadic PD patients, we 
examined gene expression levels of lysosome-associated membrane 2 (LAMP-2), a 
CMA receptor and a limiting step, and microtubule-associated protein 1 light 
chain 3 (LC3), product of which is sequentially cleaved and lipidated to form 
LC3-II as an autophagosome marker. Compared to age- and sex-matched healthy 
controls, LAMP-2 gene expression and protein levels in sporadic PD patients were 
significantly decreased, which may lead to reduced CMA activity and impaired 
fusion of autophagosome and lysosome. LC3 gene expression and LC3-II protein 
levels were significantly increased in sporadic PD patients, suggesting that 
autophagosomes are accumulated. Our findings, decreased LAMP-2 gene expression 
and increased LC3 gene expression, are consistent to the previous studies with 
dopaminergic neuronal cells in vitro and in vivo, which may contribute to the 
pathogenesis of sporadic PD by altering CMA and autophagy activities. The 
genetic causes leading to decreased LAMP-2 gene expression need further 
investigation and genetic or pharmacological restoration of LAMP-2 might be a 
novel strategy for treating PD patients.