Experimental Neurobiology 2019; 28(5): 554-567
Published online October 31, 2019
© The Korean Society for Brain and Neural Sciences
Uram Jin1,2,3†, Soo Jin Park1,2,4† and Sang Myun Park1,2,5*
1Department of Pharmacology, Ajou University School of Medicine, 2Center for Convergence Research of Neurological Disorders, Ajou University School of Medicine, Departments of 3Cardiology, 4Thoracic and Cardiovascular Surgery, Ajou University School of Medicine, 5BK21 Plus Program, Department of Biomedical Sciences, Ajou University School of Medicine, Suwon 16499, Korea
Correspondence to: *TEL: 82-31-219-5063, FAX: 82-31-219-5069
†These authors contributed equally to this work.
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Parkinson’s disease (PD) is the second most progressive neurodegenerative disorder of the aging population after Alzheimer’s disease (AD). Defects in the lysosomal systems and mitochondria have been suspected to cause the pathogenesis of PD. Nevertheless, the pathogenesis of PD remains obscure. Abnormal cholesterol metabolism is linked to numerous disorders, including atherosclerosis. The brain contains the highest level of cholesterol in the body and abnormal cholesterol metabolism links also many neurodegenerative disorders such as AD, PD, Huntington’s disease (HD), and amyotrophic lateral sclerosis (ALS). The blood brain barrier effectively prevents uptake of lipoprotein-bound cholesterol from blood circulation. Accordingly, cholesterol level in the brain is independent from that in peripheral tissues. Because cholesterol metabolism in both peripheral tissue and the brain are quite different, cholesterol metabolism associated with neurodegeneration should be examined separately from that in peripheral tissues. Here, we review and compare cholesterol metabolism in the brain and peripheral tissues. Furthermore, the relationship between alterations in cholesterol metabolism and PD pathogenesis is reviewed.