Exp Neurobiol 2013; 22(4): 283-300
Published online December 30, 2013
© The Korean Society for Brain and Neural Sciences
Hyo Eun Moon1,2,3, Seung Hee Yoon5, Yong Suk Hur6, Hyung Woo Park1,2,3, Ji Young Ha5, Kyung-Hee Kim5, Jung Hee Shim5, Seung Hyun Yoo6, Jin H. Son5, Seung Leal Paek1,2,3,8, In Keyoung Kim1, Jae Ha Hwang1, Dong Gyu Kim1, Han-Joon Kim4, Beom Seok Jeon4, Sung Sup Park7 and Sun Ha Paek1,2,3*
1Department of Neurosurgery, 2Cancer Research Institute, 3Ischemic/Hypoxic Disease Institute, Seoul National University College of Medicine, 4Department of Neurology, Seoul National University College of Medicine, Seoul 110-744, 5Department of Brain & Cognitive Sciences, College of Pharmacy, Brain Disease Research Institute, Ewha Woman’s University, Seoul 120-750, 6Department of Biochemistry, Inha University School of Medicine, Incheon 402-751, 7Department of Laboratory Medicine, Seoul National University Hospital, Seoul 110-744, Korea, 8Department of Neurosurgery, Mayo Clinic, USA
Correspondence to: *To whom correspondence should be addressed.
TEL: 82-2-2072-3993, FAX: 82-2-744-8459
Mitochondrial dysfunction in dopaminergic neurons of patients with idiopathic and familial Parkinson's disease (PD) is well known although the underlying mechanism is not clear. We established a homogeneous population of human adipose tissue-derived mesenchymal stromal cells (hAD-MSCs) from human adult patients with early-onset hereditary familial Parkin-defect PD as well as late-onset idiopathic PD by immortalizing cells with the hTERT gene to better understand the underlying mechanism of PD. The hAD-MSCs from patients with idiopathic PD were designated as "
Keywords: hTERT, hAD-MSC, immortalization, Parkinson’s disease, diagnosis