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parkin and parkinson disease

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https://www.readbyqxmd.com/read/28541509/evidence-that-phosphorylated-ubiquitin-signaling-is-involved-in-the-etiology-of-parkinson-s-disease
#1
Kahori Shiba-Fukushima, Kei-Ichi Ishikawa, Tsuyoshi Inoshita, Nana Izawa, Masashi Takanashi, Shigeto Sato, Osamu Onodera, Wado Akamatsu, Hideyuki Okano, Yuzuru Imai, Nobutaka Hattori
The ubiquitin (Ub) kinase PINK1 and the E3 Ub ligase Parkin, two gene products associated with young-onset Parkinson's disease (PD), participate in mitochondrial quality control. The phosphorylation of mitochondrial polyUb by PINK1, which is activated in a mitochondrial membrane potential (ΔΨm)-dependent manner, facilitates the mitochondrial translocation and concomitant enzymatic activation of Parkin, leading to the clearance of phospho-polyUb-tagged mitochondria via mitophagy. Thus, Ub phosphorylation is a key event in PINK1-Parkin-mediated mitophagy...
May 25, 2017: Human Molecular Genetics
https://www.readbyqxmd.com/read/28526446/thymoquinone-exerts-neuroprotective-effect-in-animal-model-of-parkinson-s-disease
#2
Seyedeh Shohreh Ebrahimi, Shahrbanoo Oryan, Esmael Izadpanah, Kambiz Hassanzadeh
Oxidative stress plays an important role in both the initiation and progression of Parkinson's disease (PD). Rotenone, an environmental toxin, induces oxidative stress and impact mitochondrial dynamics, including fission and fusion. Thymoquinone (TQ) has been reported to have antioxidant and anti-inflammatory characteristics in vitro and in vivo. TQ scavenges free radicals so prevents cell damage against oxidative agents. To evaluate the efficacy of TQ in the management of PD, male Wistar rats (8-10 months) received rotenone...
May 16, 2017: Toxicology Letters
https://www.readbyqxmd.com/read/28523222/olfaction-in-parkin-carriers-in-chinese-patients-with-parkinson-disease
#3
Ying Wang, Jian-Jun Wu, Feng-Tao Liu, Kui Chen, Chen Chen, Su-Shan Luo, Yi-Xuan Wang, Da-Ke Li, Rong-Yuan Guan, Yu-Jie Yang, Yu An, Jian Wang, Yi-Min Sun
BACKGROUND: Olfactory identification was reported to be better among PD (Parkinson disease) patients with Parkin mutations, but previous studies didn't eliminate the interference of other PD related genes on olfaction, and whether olfaction of Parkin mutations patients was better in Chinese population was still unknown. OBJECTIVE: To assess olfaction function among PD patients with Parkin mutations in Chinese population. MATERIALS AND METHODS: A total of 226 PD patients with a positive family history or an early-onset age (<50 years) were enrolled for genetic testing of PD related genes by target sequencing and multiple ligation-dependent probe amplification...
May 2017: Brain and Behavior
https://www.readbyqxmd.com/read/28511254/genetic-forms-of-parkinson-s-disease
#4
Christine Y Kim, Roy N Alcalay
One of the greatest advances in Parkinson's disease (PD) research in the past two decades has been a better understanding of PD genetics. Of the many candidate genes investigated, the best studied include LRRK2, SNCA, VPS35, Parkin, PINK1, and DJ1. The authors review the key clinical features of these monogenic forms, as well as for the prevalent risk factor gene, GBA, including the phenotype, clinical course, and treatment response. They also outline areas for future investigation: longitudinal studies of PD's clinical course, the identification of its premotor manifestations, and its specific mechanisms of pathogenicity...
April 2017: Seminars in Neurology
https://www.readbyqxmd.com/read/28507507/pink1-parkin-dependent-mitochondrial-surveillance-from-pleiotropy-to-parkinson-s-disease
#5
REVIEW
Francois Mouton-Liger, Maxime Jacoupy, Jean-Christophe Corvol, Olga Corti
Parkinson's disease (PD) is one of the most frequent neurodegenerative disease caused by the preferential, progressive degeneration of the dopaminergic (DA) neurons of the substantia nigra (SN) pars compacta. PD is characterized by a multifaceted pathological process involving protein misfolding, mitochondrial dysfunction, neuroinflammation and metabolism deregulation. The molecular mechanisms governing the complex interplay between the different facets of this process are still unknown. PARK2/Parkin and PARK6/PINK1, two genes responsible for familial forms of PD, act as a ubiquitous core signaling pathway, coupling mitochondrial stress to mitochondrial surveillance, by regulating mitochondrial dynamics, the removal of damaged mitochondrial components by mitochondria-derived vesicles, mitophagy, and mitochondrial biogenesis...
2017: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/28502045/a-clinical-and-molecular-genetic-study-of-50-families-with-autosomal-recessive-parkinsonism-revealed-known-and-novel-gene-mutations
#6
Shaghayegh Taghavi, Rita Chaouni, Abbas Tafakhori, Luis J Azcona, Saghar Ghasemi Firouzabadi, Mir Davood Omrani, Javad Jamshidi, Babak Emamalizadeh, Gholam Ali Shahidi, Mona Ahmadi, Seyed Amir Hassan Habibi, Azadeh Ahmadifard, Atena Fazeli, Marzieh Motallebi, Peyman Petramfar, Saeed Askarpour, Shiva Askarpour, Hossein Ali Shahmohammadibeni, Neda Shahmohammadibeni, Hajar Eftekhari, Amir Ehtesham Shafiei Zarneh, Saeed Mohammadihosseinabad, Mehdi Khorrami, Safa Najmi, Ahmad Chitsaz, Parasto Shokraeian, Hossein Ehsanbakhsh, Jalal Rezaeidian, Reza Ebrahimi Rad, Faranak Madadi, Monavvar Andarva, Elham Alehabib, Minoo Atakhorrami, Seyed Erfan Mortazavi, Zahra Azimzadeh, Mahdis Bayat, Amir Mohammad Besharati, Mohammad Ali Harati-Ghavi, Samareh Omidvari, Zahra Dehghani-Tafti, Faraz Mohammadi, Banafsheh Mohammad Hossein Pour, Hamid Noorollahi Moghaddam, Ehsan Esmaili Shandiz, Arman Habibi, Zahra Taherian-Esfahani, Hossein Darvish, Coro Paisán-Ruiz
In this study, the role of known Parkinson's disease (PD) genes was examined in families with autosomal recessive (AR) parkinsonism to assist with the differential diagnosis of PD. Some families without mutations in known genes were also subject to whole genome sequencing with the objective to identify novel parkinsonism-related genes. Families were selected from 4000 clinical files of patients with PD or parkinsonism. AR inheritance pattern, consanguinity, and a minimum of two affected individuals per family were used as inclusion criteria...
May 13, 2017: Molecular Neurobiology
https://www.readbyqxmd.com/read/28467897/dopamine-induces-oscillatory-activities-in-human-midbrain-neurons-with-parkin-mutations
#7
Ping Zhong, Zhixing Hu, Houbo Jiang, Zhen Yan, Jian Feng
Locomotor symptoms in Parkinson's disease (PD) are accompanied by widespread oscillatory neuronal activities in basal ganglia. Here, we show that activation of dopamine D1-class receptors elicits a large rhythmic bursting of spontaneous excitatory postsynaptic currents (sEPSCs) in midbrain neurons differentiated from induced pluripotent stem cells (iPSCs) of PD patients with parkin mutations, but not normal subjects. Overexpression of wild-type parkin, but not its PD-causing mutant, abolishes the oscillatory activities in patient neurons...
May 2, 2017: Cell Reports
https://www.readbyqxmd.com/read/28458632/the-monoamine-brainstem-reticular-formation-as-a-paradigm-for-re-defining-various-phenotypes-of-parkinson-s-disease-owing-genetic-and-anatomical-specificity
#8
REVIEW
Stefano Gambardella, Rosangela Ferese, Francesca Biagioni, Carla L Busceti, Rosa Campopiano, Anna M P Griguoli, Fiona Limanaqi, Giuseppe Novelli, Marianna Storto, Francesco Fornai
The functional anatomy of the reticular formation (RF) encompasses a constellation of brain regions which are reciprocally connected to sub-serve a variety of functions. Recent evidence indicates that neuronal degeneration within one of these regions spreads synaptically along brainstem circuitries. This is exemplified by the recruitment of various brainstem reticular nuclei in specific Parkinson's disease (PD) phenotypes, and by retrospective analysis of lethargic post-encephalitic parkinsonism. In fact, the spreading to various monoamine reticular nuclei can be associated with occurrence of specific motor and non-motor symptoms (NMS)...
2017: Frontiers in Cellular Neuroscience
https://www.readbyqxmd.com/read/28445716/trumping-neurodegeneration-targeting-common-pathways-regulated-by-autosomal-recessive-parkinson-s-disease-genes
#9
REVIEW
Laura Scott, Valina L Dawson, Ted M Dawson
Parkinson's disease (PD) is a neurodegenerative movement disorder characterized by the progressive loss of dopaminergic (DA) neurons. Most PD cases are sporadic; however, rare familial forms have been identified. Autosomal recessive PD (ARPD) results from mutations in Parkin, PINK1, DJ-1, and ATP13A2, while rare, atypical juvenile ARPD result from mutations in FBXO7, DNAJC6, SYNJ1, and PLA2G6. Studying these genes and their function has revealed mitochondrial quality control, protein degradation processes, and oxidative stress responses as common pathways underlying PD pathogenesis...
April 23, 2017: Experimental Neurology
https://www.readbyqxmd.com/read/28438176/the-pink1-p-i368n-mutation-affects-protein-stability-and-ubiquitin-kinase-activity
#10
Maya Ando, Fabienne C Fiesel, Roman Hudec, Thomas R Caulfield, Kotaro Ogaki, Paulina Górka-Skoczylas, Dariusz Koziorowski, Andrzej Friedman, Li Chen, Valina L Dawson, Ted M Dawson, Guojun Bu, Owen A Ross, Zbigniew K Wszolek, Wolfdieter Springer
BACKGROUND: Mutations in PINK1 and PARKIN are the most common causes of recessive early-onset Parkinson's disease (EOPD). Together, the mitochondrial ubiquitin (Ub) kinase PINK1 and the cytosolic E3 Ub ligase PARKIN direct a complex regulated, sequential mitochondrial quality control. Thereby, damaged mitochondria are identified and targeted to degradation in order to prevent their accumulation and eventually cell death. Homozygous or compound heterozygous loss of either gene function disrupts this protective pathway, though at different steps and by distinct mechanisms...
April 24, 2017: Molecular Neurodegeneration
https://www.readbyqxmd.com/read/28437683/pink1-and-parkin-emerging-themes-in-mitochondrial-homeostasis
#11
REVIEW
Thomas G McWilliams, Miratul Mk Muqit
The Parkinson's disease (PD)-associated protein kinase, PTEN-induced putative kinase1 (PINK1), and ubiquitin E3 ligase, Parkin function in a common signalling pathway known to regulate mitochondrial network homeostasis and quality control, including mitophagy. The multistep activation of this pathway, as well as an unexpected convergence between the post-translational modifications of ubiquitylation and phosphorylation, has added breadth to our understanding of cellular damage responses during human disease...
April 21, 2017: Current Opinion in Cell Biology
https://www.readbyqxmd.com/read/28435104/drosophila-pink1-and-parkin-loss-of-function-mutants-display-a-range-of-non-motor-parkinson-s-disease-phenotypes
#12
Hannah Julienne, Edgar Buhl, David S Leslie, James J L Hodge
Parkinson's disease (PD) is more commonly associated with its motor symptoms and the related degeneration of dopamine (DA) neurons. However, it is becoming increasingly clear that PD patients also display a wide range of non-motor symptoms, including memory deficits and disruptions of their sleep-wake cycles. These have a large impact on their quality of life, and often precede the onset of motor symptoms, but their etiology is poorly understood. The fruit fly Drosophila has already been successfully used to model PD, and has been used extensively to study relevant non-motor behaviours in other contexts, but little attention has yet been paid to modelling non-motor symptoms of PD in this genetically tractable organism...
April 21, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28433685/p62-mediated-mitochondrial-clustering-attenuates-apoptosis-induced-by-mitochondrial-depolarization
#13
Bin Xiao, Xiao Deng, Grace G Y Lim, Wei Zhou, Wuan-Ting Saw, Zhi Dong Zhou, Kah-Leong Lim, Eng-King Tan
Parkin/PINK1-mediated mitophagy is implicated in the pathogenesis of Parkinson's disease (PD). Prior to elimination of damaged mitochondria, Parkin translocates to mitochondria and induces mitochondrial clustering. While the mechanism of PINK1-dependent Parkin redistribution to mitochondria is now becoming clear, the role of mitochondrial clustering has been less well understood. In our study, we found that loss of p62 disrupted mitochondrial aggregation and specifically sensitized Parkin-expressing cells to apoptosis induced by mitochondrial depolarization...
April 19, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28432765/nature-s-parkin-experiment-nix-a-novel-protective-mechanism-in-parkinson-s-disease
#14
Diana A Olszewska, Tim Lynch
No abstract text is available yet for this article.
April 22, 2017: Movement Disorders: Official Journal of the Movement Disorder Society
https://www.readbyqxmd.com/read/28430587/parkin-regulates-translesion-dna-synthesis-in-response-to-uv-radiation
#15
Xuefei Zhu, Xiaolu Ma, Yingfeng Tu, Min Huang, Hongmei Liu, Fengli Wang, Juanjuan Gong, Jiuqiang Wang, Xiaoling Li, Qian Chen, Hongyan Shen, Shu Zhu, Yun Wang, Yang Liu, Caixia Guo, Tie-Shan Tang
Deficiency of Parkin is a major cause of early-onset Parkinson's disease (PD). Notably, PD patients also exhibit a significantly higher risk in melanoma and other skin tumors, while the mechanism remains largely unknown. In this study, we show that depletion of Parkin causes compromised cell viability and genome stability after ultraviolet (UV) radiation. We demonstrate that Parkin promotes efficient Rad18-dependent proliferating cell nuclear antigen (PCNA) monoubiquitination by facilitating the formation of Replication protein A (RPA)-coated ssDNA upon UV radiation...
April 5, 2017: Oncotarget
https://www.readbyqxmd.com/read/28424751/levodopa-responsive-parkinsonism-in-patients-with-hemochromatosis-case-presentation-and-literature-review
#16
Tarun Girotra, Abhimanyu Mahajan, Christos Sidiropoulos
Hemochromatosis is an autosomal recessive disorder which leads to abnormal iron deposition in the parenchyma of multiple organs causing tissue damage. Accumulation of iron in the brain has been postulated to be associated with several neurodegenerative diseases including Parkinson's disease. The excess iron promotes Parkin and α-synuclein aggregation in the neurons. Excess iron has also been noted in substantia nigra on MRI especially using susceptibility weighted imaging in patients with Parkinson's disease...
2017: Case Reports in Neurological Medicine
https://www.readbyqxmd.com/read/28408429/ubiquitin-and-parkinson-s-disease-through-the-looking-glass-of-genetics
#17
REVIEW
Helen Walden, Miratul M K Muqit
Biochemical alterations found in the brains of Parkinson's disease (PD) patients indicate that cellular stress is a major driver of dopaminergic neuronal loss. Oxidative stress, mitochondrial dysfunction, and ER stress lead to impairment of the homeostatic regulation of protein quality control pathways with a consequent increase in protein misfolding and aggregation and failure of the protein degradation machinery. Ubiquitin signalling plays a central role in protein quality control; however, prior to genetic advances, the detailed mechanisms of how impairment in the ubiquitin system was linked to PD remained mysterious...
April 13, 2017: Biochemical Journal
https://www.readbyqxmd.com/read/28407521/genetic-or-pharmacological-activation-of-the-drosophila-pgc-1%C3%AE-ortholog-spargel-rescues-the-disease-phenotypes-of-genetic-models-of-parkinson-s-disease
#18
Chee-Hoe Ng, Adeline H Basil, Liting Hang, Royston Tan, Kian-Leong Goh, Sharon O'Neill, Xiaodong Zhang, Fengwei Yu, Kah-Leong Lim
Despite intensive research, the etiology of Parkinson's disease (PD) remains poorly understood and the disease remains incurable. However, compelling evidence gathered over decades of research strongly support a role for mitochondrial dysfunction in PD pathogenesis. Related to this, PGC-1α, a key regulator of mitochondrial biogenesis, has recently been proposed to be an attractive target for intervention in PD. Here, we showed that silencing of expression of the Drosophila PGC-1α ortholog spargel results in PD-related phenotypes in flies and also seem to negate the effects of AMPK activation, which we have previously demonstrated to be neuroprotective, that is, AMPK-mediated neuroprotection appears to require PGC-1α...
March 18, 2017: Neurobiology of Aging
https://www.readbyqxmd.com/read/28399880/quantitative-proteomic-analysis-of-parkin-substrates-in-drosophila-neurons
#19
Aitor Martinez, Benoit Lectez, Juanma Ramirez, Oliver Popp, James D Sutherland, Sylvie Urbé, Gunnar Dittmar, Michael J Clague, Ugo Mayor
BACKGROUND: Parkin (PARK2) is an E3 ubiquitin ligase that is commonly mutated in Familial Parkinson's Disease (PD). In cell culture models, Parkin is recruited to acutely depolarised mitochondria by PINK1. PINK1 activates Parkin activity leading to ubiquitination of multiple proteins, which in turn promotes clearance of mitochondria by mitophagy. Many substrates have been identified using cell culture models in combination with depolarising drugs or proteasome inhibitors, but not in more physiological settings...
April 11, 2017: Molecular Neurodegeneration
https://www.readbyqxmd.com/read/28395174/loss-of-parkin-reduces-inflammatory-arthritis-by-inhibiting-p53-degradation
#20
Yu Yeon Jung, Dong Ju Son, Hye Lim Lee, Dae Hwan Kim, Min Jong Song, Young Wan Ham, Youngsoo Kim, Sang Bae Han, Mi Hee Park, Jin Tae Hong
Parkin is associated with various inflammatory diseases, including Parkinson's disease (PD) and rheumatoid arthritis (RA). However, the precise role of Parkin in RA is unclear. The present study addressed this issue by comparing the development of RA between non-transgenic (non-Tg) mice and PARK2 knockout (KO) mice. We found that cyclooxygenase-2 and inducible nitric oxide synthase expression and nuclear factor-κB activity were reduced but p53 activation was increased in PARK2 KO as compared to non-Tg mice...
April 5, 2017: Redox Biology
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