Pick Topic
Review Topic
List Experts
Examine Expert
Save Expert
  Site Guide ··   
Parkinson Disease: HELP
Articles by Tian-Hong Pan
Based on 4 articles published since 2010
(Why 4 articles?)
||||

Between 2010 and 2020, Tianhong Pan wrote the following 4 articles about Parkinson Disease.
 
+ Citations + Abstracts
1 Review The association between Parkinson's disease and melanoma. 2011

Pan, Tianhong / Li, Xinqun / Jankovic, Joseph. ·Diana Helis Henry Medical Research Foundation, New Orleans, LA, USA. ·Int J Cancer · Pubmed #21207412.

ABSTRACT: Parkinson's disease (PD) is a neurodegenerative disorder characterized by a loss of melanin-positive, dopaminergic neurons in the substantia nigra. Although there is convincing epidemiologic evidence of a negative association between PD and most cancers, a notable exception to this is that melanoma, a malignant tumor of melanin-producing cells in skin, occurs with higher-than-expected frequency among subjects with PD and that melanoma patients are more likely to have PD. A clear biological explanation for this epidemiological observation is lacking. Here, we present a comprehensive review of published literature exploring the association between PD and melanoma. On the basis of published findings, we conclude that (i) changes in pigmentation including melanin synthesis and/or melanin synthesis enzymes, such as tyrosinase and tyrosine hydroxylase, play important roles in altered vulnerability for both PD and melanoma; (ii) changes of PD-related genes such as Parkin, LRRK2 and α-synuclein may increase the risk of melanoma; (iii) changes in some low-penetrance genes such as cytochrome p450 debrisoquine hydroxylase locus, glutathione S-transferase M1 and vitamin D receptor could increase the risk for both PD and melanoma and (iv) impaired autophagy in both PD and melanoma could also explain the association between PD and melanoma. Future studies are required to address whether altered pigmentation, PD- or melanoma-related gene changes and/or changes in autophagy function induce oncogenesis or apoptosis. From a clinical point of view, early diagnosis of melanoma in PD patients is critical and can be enhanced by periodic dermatological surveillance, including skin biopsies.

2 Article Neuroprotection by Orexin-A via HIF-1α induction in a cellular model of Parkinson's disease. 2014

Feng, Ya / Liu, Te / Li, Xin-Qun / Liu, Ye / Zhu, Xiao-Ying / Jankovic, Joseph / Pan, Tian-Hong / Wu, Yun-Cheng. ·Department of Neurology, Shanghai First People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, PR China. · Shanghai Geriatric Institute of Chinese Medicine, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200031, PR China. · Department of Experimental Therapeutics, M.D. Anderson Cancer Center, Houston, TX 77030, USA. · Parkinson's Disease Center and Movement Disorders Clinic, Department of Neurology, Baylor College of Medicine, Houston, TX 77030, USA. · Parkinson's Disease Center and Movement Disorders Clinic, Department of Neurology, Baylor College of Medicine, Houston, TX 77030, USA. Electronic address: Tpan1@mdanderson.org. · Department of Neurology, Shanghai First People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, PR China. Electronic address: yunchw@medmail.com.cn. ·Neurosci Lett · Pubmed #25038418.

ABSTRACT: Orexin-A, a neuropeptide secreted by hypothalamic neurons, may be neuroprotective in many neurological conditions such as cerebral ischaemia. One mechanism postulated to be involved in the neuroprotection by Orexin-A is the induction of hypoxia inducible factor 1 alpha (HIF-1α). Parkinson's disease (PD) is a progressive neurodegenerative disorder and mitochondrial dysfunction has been demonstrated to play a role in its pathogenesis. Mitochondrial dysfunction may cause reduction of O2 consumption and subsequently activate prolyl hydroxylase, which leads to decreased level of HIF-1α. In this study, we used MPP(+)-treated SH-SY5Y cells as an in vitro cellular model of PD to test the role of Orexin-A as an inducer of HIF-1α. Our results showed that Orexin-A not only induced HIF-1α but also activated downstream targets of HIF-1α, such as vascular endothelial growth factor and erythropoietin. Thus, Orexin-A treatment attenuated MPP(+)-induced cell injury and this effect was blocked when HIF-1α was suppressed. Hence, we conclude that induction of HIF-1α is one of the mechanisms involved in the neuroprotection by Orexin-A.

3 Article Effects of deep brain stimulation in relatively young-onset multiple system atrophy Parkinsonism. 2014

Zhu, Xiao-Ying / Pan, Tian-Hong / Ondo, William G / Jimenez-Shahed, Joohi / Wu, Yun-Cheng. ·Department of Neurology, Shanghai First People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, PR China. · Parkinson's Disease Center and Movement Disorder Clinic, Department of Neurology, Baylor College of Medicine, Houston 77030, TX, USA. · Department of Neurology, University of Texas Health Science Center Houston, Houston, TX, USA. · Department of Neurology, Shanghai First People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, PR China. Electronic address: yunchw@medmail.com.cn. ·J Neurol Sci · Pubmed #24831987.

ABSTRACT: OBJECTIVE: The aim of this study was to analyze outcomes after 1 year of bilateral STN deep brain stimulation (DBS) in relatively young-onset patients with multiple system atrophy-Parkinsonism (MSA-P). BACKGROUND: The efficacy of DBS has been demonstrated in idiopathic Parkinson's disease. However, the experience with DBS in relatively young-onset MSA-P is limited and controversial. METHODS: Information about the demographic and clinical data from five MSA patients treated with STN DBS was entered into a database and analyzed. RESULTS: Five patients with relatively young-onset MSA (mean age at onset 42.2±2.2 years, 3 women, 2 men) have been treated with bilateral STN stimulators, the mean duration between DBS surgery and disease onset was 7.0±3.5 years. All of the patients had dyskinesia and postural instability, and subjective benefit from levodopa. During the 6 months after surgery, the clinical status of three patients improved with a decrease of dyskinesia. However, by 1 year, the symptoms reappeared and progressed in all patients. Overall, the mean "off" medication UPDRS-III score worsened 23.5±15.3 1 year after surgery and the levodopa dosage was not reduced. CONCLUSIONS: This data does not support the use of STN DBS for relatively young-onset MSA-P.

4 Article The role of alpha-synuclein in melanin synthesis in melanoma and dopaminergic neuronal cells. 2012

Pan, Tianhong / Zhu, Julie / Hwu, Wen-Jen / Jankovic, Joseph. ·Neurology Department, Parkinson Disease Research Laboratory, Baylor College of Medicine, Houston, Texas, USA. tpan@bcm.edu ·PLoS One · Pubmed #23028833.

ABSTRACT: The relatively high co-occurrence of Parkinson's disease (PD) and melanoma has been established by a large number of epidemiological studies. However, a clear biological explanation for this finding is still lacking. Ultra-violet radiation (UVR)-induced skin melanin synthesis is a defense mechanism against UVR-induced damage relevant to the initiation of melanoma, whereas, increased neuromelanin (NM), the melanin synthesized in dopaminergic neurons, may enhance the susceptibility to oxidative stress-induced neuronal injury relevant to PD. SNCA is a PD-causing gene coding for alpha-Synuclein (α-Syn) that expresses not only in brain, but also in skin as well as in tumors, such as melanoma. The findings that α-Syn can interact with tyrosinase (TYR) and inhibit tyrosine hydroxylase (TH), both of which are enzymes involved in the biosynthesis of melanin and dopamine (DA), led us to propose that α-Syn may participate in the regulation of melanin synthesis. In this study, by applying ultraviolet B (UVB) light, a physiologically relevant stimulus of melanogenesis, we detected melanin synthesis in A375 and SK-MEL-28 melanoma cells and in SH-SY5Y and PC12 dopaminergic neuronal cells and determined effects of α-Syn on melanin synthesis. Our results showed that UVB light exposure increased melanin synthesis in all 4 cell lines. However, we found that α-Syn expression reduced UVB light-induced increase of melanin synthesis and that melanin content was lower when melanoma cells were expressed with α-Syn, indicating that α-Syn may have inhibitory effects on melanin synthesis in melanoma cells. Different from melanoma cells, the melanin content was higher in α-Syn-over-expressed dopaminergic neuronal SH-SY5Y and PC12 cells, cellular models of PD, than that in non-α-Syn-expressed control cells. We concluded that α-Syn could be one of the points responsible for the positive association between PD and melanoma via its differential roles in melanin synthesis in melanoma cells and in dopaminergic neuronal cells.