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Parkinson Disease: HELP
Articles by Yeojin Bang
Based on 3 articles published since 2010
(Why 3 articles?)
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Between 2010 and 2020, Yeojin Bang wrote the following 3 articles about Parkinson Disease.
 
+ Citations + Abstracts
1 Review Abnormal hippocampal neurogenesis in Parkinson's disease: relevance to a new therapeutic target for depression with Parkinson's disease. 2018

Lim, Juhee / Bang, Yeojin / Choi, Hyun Jin. ·College of Pharmacy and Institute of Pharmaceutical Sciences, CHA University, Seongnam-si, Gyeonggi-do, 13488, Republic of Korea. · College of Pharmacy and Institute of Pharmaceutical Sciences, CHA University, Seongnam-si, Gyeonggi-do, 13488, Republic of Korea. hjchoi3@cha.ac.kr. ·Arch Pharm Res · Pubmed #30136247.

ABSTRACT: Parkinson's disease (PD) is a common progressive neurodegenerative disorder characterized by motor dysfunction, including bradykinesia, tremor, rigidity, and postural instability. Recent clinical findings recognize PD as a complex disease with diverse neuropsychiatric complications. Depression is the most frequent non-motor psychiatric symptom experienced in PD, and it is associated with poor quality of life. While the pathophysiology of PD-associated depression is not directly related to neurodegenerative processes in the substantia nigra, underlying mechanisms remain unclear and there are few symptomatic treatments. Altered adult hippocampal neurogenesis is considered crucial for the development and treatment of depression. In genetic animal models and human postmortem studies of PD, severely impaired adult neurogenesis has been observed, with patients showing hippocampal atrophy and disrupted hippocampal neurogenesis. Because adult newborn neurons appear to exert various functions, which relate to non-motor symptoms observed in PD, there might be a close correlation between malformation of newborn neurons in the adult hippocampus and depressive symptoms. Here, we discuss current concepts regarding impaired hippocampal neurogenesis and non-motor symptoms of PD, and review PD-associated pathophysiological factors regulating neurogenesis, including inflammatory signaling and autophagy. We present a novel framework for targeting adult hippocampal neurogenesis, which could provide a promising treatment for PD-associated depression.

2 Article LRRK2 G2019S Induces Anxiety/Depression-like Behavior before the Onset of Motor Dysfunction with 5-HT 2018

Lim, Juhee / Bang, Yeojin / Choi, Jong-Hyun / Han, Arum / Kwon, Min-Soo / Liu, Kwang Hyeon / Choi, Hyun Jin. ·College of Pharmacy and Institute of Pharmaceutical Sciences. · Department of Pharmacology, School of Medicine, Cha University, Seongnam, Gyeonggi-do 13488, Republic of Korea, and. · BK21 Plus Kyungpook National University Multi-Omics Based Creative Drug Research Team, College of Pharmacy and Research Institute of Pharmaceutical Sciences, Kyungpook National University, Daegu 41566, Republic of Korea. · College of Pharmacy and Institute of Pharmaceutical Sciences, hjchoi3@cha.ac.kr. ·J Neurosci · Pubmed #29305532.

ABSTRACT: Mutations in the

3 Article LRRK2 interferes with aggresome formation for autophagic clearance. 2016

Bang, Yeojin / Kim, Kwang-Soo / Seol, Wongi / Choi, Hyun Jin. ·College of Pharmacy and Institute of Pharmaceutical Sciences, CHA University, Seongnam13488, South Korea; College of Pharmacy, Chonnam National University, Gwangju 61186, South Korea; College of Pharmacy, Chungbuk National University, Cheongju 28644, South Korea. · Molecular Neurobiology Laboratory, McLean Hospital, Harvard Medical School, Belmont, MA 02478, USA. · InAm Neuroscience Research Center, Wonkwang University, Sanbon Hospital, Gunpo, 15865, South Korea. · College of Pharmacy and Institute of Pharmaceutical Sciences, CHA University, Seongnam13488, South Korea. Electronic address: hjchoi3@cha.ac.kr. ·Mol Cell Neurosci · Pubmed #27364102.

ABSTRACT: Autosomal-dominant mutations in the gene encoding leucine-rich repeat kinase 2 (LRRK2) account for the most common monogenic form of Parkinson's disease (PD). A link between autophagy dysregulation and LRRK2 has consistently been reported, but it remains poorly defined which step is targeted by LRRK2. Here, we sought to examine the effect of LRRK2 on the sequestration and degradation of aggregated protein complexes for autophagic clearance. Because two major intracellular protein degradation systems, the ubiquitin proteasome system and the autophagy, are functionally coupled, proteasome inhibition is suggested to activate autophagy. So, we induced protein quality control-associated autophagy using the proteasome inhibitor MG132 in differentiated SH-SY5Y cells and mice expressing G2019S mutant LRRK2 to uncover how the autophagy pathway is affected by LRRK2. We found that LRRK2 disrupted aggresome formation for autophagic clearance of accumulated protein aggregates. Specifically, we observed the following in differentiated SH-SY5Y cells with overexpressed wild-type and G2019S LRRK2: 1) large, clear, perinuclear aggresomes were not detected under MG132, instead, much smaller aggregates were broadly distributed in the cytosol; 2) enhanced accumulation of LC3-II and p62/ubiquitin-positive protein inclusions were noted; and 3) protein aggregates were not cleared even after a recovery period, which exacerbated the MG132-induced cytotoxicity. Notably, higher protein accumulation was detected in the brains of G2019S transgenic mice than in the brains of littermate control mice under proteasome inhibition. Our present findings provide insight into the precise mechanisms that underlie autophagy dysregulation in the brains of patients with PD with LRRK2 mutations.