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parkinson's disease and mitochondria

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https://www.readbyqxmd.com/read/29341130/mitochondrial-function-and-autophagy-integrating-proteotoxic-redox-and-metabolic-stress-in-parkinson-s-disease
#1
REVIEW
Jianhua Zhang, M Lillian Culp, Jason G Craver, Victor Darley-Usmar
Parkinson's disease (PD) is a movement disorder with widespread neurodegeneration in the brain. Significant oxidative, reductive, metabolic, and proteotoxic alterations have been observed in PD postmortem brains. The alterations of mitochondrial function resulting in decreased bioenergetic health is important and needs to be further examined to help develop biomarkers for PD severity and prognosis. It is now becoming clear that multiple hits on metabolic and signaling pathways are likely to exacerbate PD pathogenesis...
January 17, 2018: Journal of Neurochemistry
https://www.readbyqxmd.com/read/29335845/carnosic-acid-as-a-promising-agent-in-protecting-mitochondria-of-brain-cells
#2
REVIEW
Marcos Roberto de Oliveira
Carnosic acid (CA; C20H28O4), a phenolic diterpene characterized as an ortho-dihydroquinone-type molecule, is a pro-electrophile agent that becomes an electrophile after reacting with free radicals. The electrophile generated from CA interacts with and activates the nuclear factor erythroid 2-related factor 2 (Nrf2) transcription factor, which is a major modulator of redox biology in mammalian cells. CA induces antioxidant and anti-inflammatory effects in several cell types, as observed in both in vitro and in vivo experimental models...
January 15, 2018: Molecular Neurobiology
https://www.readbyqxmd.com/read/29325568/pink1-import-regulation-a-fine-system-to-convey-mitochondrial-stress-to-the-cytosol
#3
REVIEW
Shiori Sekine, Richard J Youle
Insights from inherited forms of parkinsonism suggest that insufficient mitophagy may be one etiology of the disease. PINK1/Parkin-dependent mitophagy, which helps maintain a healthy mitochondrial network, is initiated by activation of the PINK1 kinase specifically on damaged mitochondria. Recent investigation of this process reveals that import of PINK1 into mitochondria is regulated and yields a stress-sensing mechanism. In this review, we focus on the mechanisms of mitochondrial stress-dependent PINK1 activation that is exerted by regulated import of PINK1 into different mitochondrial compartments and how this offers strategies to pharmacologically activate the PINK1/Parkin pathway...
January 10, 2018: BMC Biology
https://www.readbyqxmd.com/read/29316798/regulation-of-mitophagy-by-the-ubiquitin-pathway-in-neurodegenerative-diseases
#4
Shyamal Desai, Meredith Juncker, Catherine Kim
Mitophagy is a cellular process by which dysfunctional mitochondria are degraded via autophagy. Increasing empirical evidence proposes that this mitochondrial quality-control mechanism is defective in neurons of patients with various neurodegenerative diseases such as Ataxia Telangiectasia, Alzheimer's disease, Parkinson's disease, and Amyotrophic Lateral Sclerosis. Accumulation of defective mitochondria and the production of reactive oxygen species due to defective mitophagy have been identified as causes underlying neurodegenerative disease pathogenesis...
January 1, 2018: Experimental Biology and Medicine
https://www.readbyqxmd.com/read/29315581/parkinson-disease-related-dj-1-modulates-the-expression-of-uncoupling-protein-4-against-oxidative-stress
#5
Shaoqing Xu, Xiaodong Yang, Yiwei Qian, Qin Xiao
Loss of function mutations of DJ-1 (PARK7) have been linked to the pathogenesis of Parkinson disease (PD). Antioxidative stress is one of the multi-protective functions of DJ-1, and oxidation of cysteine 106 (Cys106) has been proposed to regulate the protective activity of DJ-1. Uncoupling protein 4 (UCP4) is located in the inner membrane of mitochondria and functions to protect against oxidative stress. In this study, we used neuronal (SH-SY5Y) cells and DJ-1 knockout (KO) mice to elucidate whether DJ-1 regulated oxidative stress via modulating the expression of UCP4, and the underlying mechanism...
January 8, 2018: Journal of Neurochemistry
https://www.readbyqxmd.com/read/29310663/%C3%AE-synuclein-accumulation-and-gba-deficiency-due-to-l444p-gba-mutation-contributes-to-mptp-induced-parkinsonism
#6
Seung Pil Yun, Donghoon Kim, Sangjune Kim, SangMin Kim, Senthilkumar S Karuppagounder, Seung-Hwan Kwon, Saebom Lee, Tae-In Kam, Suhyun Lee, Sangwoo Ham, Jae Hong Park, Valina L Dawson, Ted M Dawson, Yunjong Lee, Han Seok Ko
BACKGROUND: Mutations in glucocerebrosidase (GBA) cause Gaucher disease (GD) and increase the risk of developing Parkinson's disease (PD) and Dementia with Lewy Bodies (DLB). Since both genetic and environmental factors contribute to the pathogenesis of sporadic PD, we investigated the susceptibility of nigrostriatal dopamine (DA) neurons in L444P GBA heterozygous knock-in (GBA +/L444P ) mice to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a selective dopaminergic mitochondrial neurotoxin...
January 8, 2018: Molecular Neurodegeneration
https://www.readbyqxmd.com/read/29290944/mitochondrial-targeted-hsp90-inhibitor-gamitrinib-tpp-g-tpp-induces-pink1-parkin-dependent-mitophagy
#7
Fabienne C Fiesel, Elle D James, Roman Hudec, Wolfdieter Springer
Loss-of-function mutations in PINK1 or PARKIN are associated with early-onset Parkinson's disease. Upon mitochondrial stress, PINK1 and Parkin together mediate a response that protects cells from the accumulation of harmful, damaged mitochondria. PINK1, the upstream kinase accumulates on the mitochondrial surface and recruits the E3 ubiquitin ligase Parkin on site to ubiquitylate substrate proteins. The joint activity of both to generate phosphorylated poly-ubiquitin chains on the mitochondrial surface induces the recruitment of autophagy receptors and eventually whole organelles are cleared by autophagy...
December 5, 2017: Oncotarget
https://www.readbyqxmd.com/read/29286376/in-vitro-and-in-vivo-detection-of-mitophagy-in-human-cells-c-elegans-and-mice
#8
Evandro F Fang, Konstantinos Palikaras, Nuo Sun, Elayne M Fivenson, Ryan D Spangler, Jesse S Kerr, Stephanie A Cordonnier, Yujun Hou, Eszter Dombi, Henok Kassahun, Nektarios Tavernarakis, Joanna Poulton, Hilde Nilsen, Vilhelm A Bohr
Mitochondria are the powerhouses of cells and produce cellular energy in the form of ATP. Mitochondrial dysfunction contributes to biological aging and a wide variety of disorders including metabolic diseases, premature aging syndromes, and neurodegenerative diseases such as Alzheimer's disease (AD) and Parkinson's disease (PD). Maintenance of mitochondrial health depends on mitochondrial biogenesis and the efficient clearance of dysfunctional mitochondria through mitophagy. Experimental methods to accurately detect autophagy/mitophagy, especially in animal models, have been challenging to develop...
November 22, 2017: Journal of Visualized Experiments: JoVE
https://www.readbyqxmd.com/read/29260454/neuroprotective-effect-of-treadmill-exercise-possibly-via-regulation-of-lysosomal-degradation-molecules-in-mice-with-pharmacologically-induced-parkinson-s-disease
#9
Dong-Joo Hwang, Jung-Hoon Koo, Ki-Cheon Kwon, Dong-Hoon Choi, Sung-Deuk Shin, Jae-Hoon Jeong, Hyun-Seob Um, Joon-Yong Cho
Dysfunction of mitophagy, which is a selective degradation of defective mitochondria for quality control, is known to be implicated in the pathogenesis of Parkinson's disease (PD). However, how treadmill exercise (TE) regulates mitophagy-related molecules in PD remains to be elucidated. Therefore, we aimed to investigate how TE regulates α-synuclein (α-syn)-induced neurotoxicity and mitophagy-related molecules in the nigro-striatal region of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-mice. Our data showed that TE exhibited a significant restoration of tyrosine hydroxylase and motor coordination with suppression of α-syn expression, hallmarks of PD, possibly via up-regulation of lysosomal degradation molecules, LAMP-2 and cathepsin L, with down-regulation of p62, LC3-II/LC3-I ratio, PINK1 and parkin in the substantia nigra of MPTP mice...
December 19, 2017: Journal of Physiological Sciences: JPS
https://www.readbyqxmd.com/read/29234100/a-bi-fluorescence-complementation-system-to-detect-associations-between-the-endoplasmic-reticulum-and-mitochondria
#10
Mark Harmon, Philip Larkman, Giles Hardingham, Mandy Jackson, Paul Skehel
Close contacts between the endoplasmic reticulum membrane and the mitochondrial outer membrane facilitate efficient transfer of lipids between the organelles and coordinate Ca2+ signalling and stress responses. Changes to this coupling is associated with a number of metabolic disorders and neurodegenerative diseases including Alzheimer's, Parkinson's and motor neuron disease. The distance between the two membranes at regions of close apposition is below the resolution of conventional light microscopy, which makes analysis of these interactions challenging...
December 12, 2017: Scientific Reports
https://www.readbyqxmd.com/read/29228971/alpha-synuclein-oligomer-selective-antibodies-reduce-intracellular-accumulation-and-mitochondrial-impairment-in-alpha-synuclein-exposed-astrocytes
#11
Gabriel Gustafsson, Veronica Lindström, Jinar Rostami, Eva Nordström, Lars Lannfelt, Joakim Bergström, Martin Ingelsson, Anna Erlandsson
BACKGROUND: Due to its neurotoxic properties, oligomeric alpha-synuclein (α-syn) has been suggested as an attractive target for passive immunization against Parkinson's disease (PD). In mouse models of PD, antibody treatment has been shown to lower the levels of pathogenic α-syn species, including oligomers, although the mechanisms of action remain unknown. We have previously shown that astrocytes rapidly engulf α-syn oligomers that are intracellularly stored, rather than degraded, resulting in impaired mitochondria...
December 11, 2017: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/29228015/development-of-an-iron-selective-antioxidant-probe-with-protective-effects-on-neuronal-function
#12
Olimpo García-Beltrán, Natalia P Mena, Pabla Aguirre, Germán Barriga-González, Antonio Galdámez, Edgar Nagles, Tatiana Adasme, Cecilia Hidalgo, Marco T Núñez
Iron accumulation, oxidative stress and calcium signaling dysregulation are common pathognomonic signs of several neurodegenerative diseases, including Parkinson´s and Alzheimer's diseases, Friedreich ataxia and Huntington's disease. Given their therapeutic potential, the identification of multifunctional compounds that suppress these damaging features is highly desirable. Here, we report the synthesis and characterization of N-(1,3-dihydroxy-2-(hydroxymethyl)propan-2-yl)-2-(7-hydroxy-2-oxo-2H-chromen-4-yl)acetamide, named CT51, which exhibited potent free radical neutralizing activity both in vitro and in cells...
2017: PloS One
https://www.readbyqxmd.com/read/29225013/succinate-dehydrogenase-prospect-for-neurodegenerative-diseases
#13
REVIEW
Mohammad Jodeiri Farshbaf, Abbas Kiani-Esfahani
Onset of Alzheimer's, Parkinson's and Huntington's diseases as neurodegenerative disorders is increased by age. Alleviation of clinical symptoms and protection of neurons against degeneration are the main aspects of researches to establish new therapeutic strategies. Many studies have shown that mitochondria play crucial roles in high energy demand tissues like brain. Impairments in mitochondrial activity and physiology can makes neurons vulnerable to stress and degeneration. Succinate dehydrogenase (SDH) connects tricarboxylic cycle to the electron transport chain...
December 7, 2017: Mitochondrion
https://www.readbyqxmd.com/read/29222404/lack-of-parkin-anticipates-the-phenotype-and-affects-mitochondrial-morphology-and-mtdna-levels-in-a-mouse-model-of-parkinson-s-disease
#14
Milena Pinto, Nadee Nissanka, Carlos T Moraes
PARK2 is the most common gene mutated in monogenic recessive familial cases of Parkinson's disease (PD). Pathogenic mutations cause a loss of function of the encoded protein Parkin. ParkinKO mice, however, poorly represent human PD symptoms as they only exhibit mild motor phenotypes, minor dopamine metabolism abnormalities, and no signs of dopaminergic neurodegeneration. Parkin has been shown to participate in mitochondrial turnover, by targeting damaged mitochondria, with low membrane potential, to mitophagy...
December 8, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/29215849/-study-of-mitochondrial-dysfunction-using-cytoplasmic-hybrid
#15
V V Sinyov, M A Sazonova, V P Karagodin, A I Ryzhkova, E V Galitsyna, A A Melnichenko, N A Demakova, T P Shkurat, I A Sobenin, A N Orekhov
Aim. This review article describes literature sources devoted to the investigation of mitochondrial dysfunction using cytoplasmic hybrids (cybrids). The presented studies were carried out on cultures of cybrid cell lines HL60, MOL T-4, A549, 143B, HeLa, Arpe-19, HEK-293, SH-SY5Y and NT2. According to the analysis of scientific world literature, some of the most promising models for studying mitochondrial dysfunction are cell cultures without mitochondria (rho0) and cytoplasmic hybrids containing one or several mutations of mitochondrial genome...
April 2017: Patologicheskaia Fiziologiia i èksperimental'naia Terapiia
https://www.readbyqxmd.com/read/29207041/mitochondria-mediated-damage-to-dopaminergic-neurons-in-parkinson-s-disease-review
#16
Xiao-Liang Liu, Ying-Di Wang, Xiu-Ming Yu, Da-Wei Li, Guang-Ren Li
Mitochondria are important organelles in virtually all eukaryotic cells, and are involved in a wide range of physiological and pathophysiological processes. Besides the generation of cellular energy in the form of adenosine triphosphate, mitochondria are also involved in calcium homeostasis, reactive oxygen species production and the activation of the intrinsic cell death pathway, thus determining cell survival and death. Mitochondrial abnormalities have been implicated in a wide range of disorders, including neurodegenerative disease such as Parkinson's disease (PD), and considered as a primary cause and central event responsible for the progressive loss of dopaminergic neurons in PD...
November 16, 2017: International Journal of Molecular Medicine
https://www.readbyqxmd.com/read/29204154/mitochondria-a-common-target-for-genetic-mutations-and-environmental-toxicants-in-parkinson-s-disease
#17
REVIEW
Martin P Helley, Jennifer Pinnell, Carolina Sportelli, Kim Tieu
Parkinson's disease (PD) is a devastating neurological movement disorder. Since its first discovery 200 years ago, genetic and environmental factors have been identified to play a role in PD development and progression. Although genetic studies have been the predominant driving force in PD research over the last few decades, currently only a small fraction of PD cases can be directly linked to monogenic mutations. The remaining cases have been attributed to other risk associated genes, environmental exposures and gene-environment interactions, making PD a multifactorial disorder with a complex etiology...
2017: Frontiers in Genetics
https://www.readbyqxmd.com/read/29204109/intracellular-cholesterol-trafficking-and-impact-in-neurodegeneration
#18
REVIEW
Fabian Arenas, Carmen Garcia-Ruiz, Jose C Fernandez-Checa
Cholesterol is a critical component of membrane bilayers where it plays key structural and functional roles by regulating the activity of diverse signaling platforms and pathways. Particularly enriched in brain, cholesterol homeostasis in this organ is singular with respect to other tissues and exhibits a heterogeneous regulation in distinct brain cell populations. Due to the key role of cholesterol in brain physiology and function, alterations in cholesterol homeostasis and levels have been linked to brain diseases and neurodegeneration...
2017: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/29189163/alpha-synuclein-proteotoxicity-and-parkinson-s-disease-search-for-neuroprotective-therapy
#19
Upasana Ganguly, Sankha Shubhra Chakrabarti, Upinder Kaur, Anwesha Mukherjee, Sasanka Chakrabarti
There is a growing body of evidence in animal and cell based models of Parkinson's disease (PD) to suggest that overexpression and / or abnormal accumulation and aggregation of α-synuclein can trigger neuronal death. This important role of α-synuclein in PD pathogenesis is supported by the fact that duplication, triplication and mutations of α-synuclein gene cause familial forms of PD. The overexpression and accumulation of α-synuclein within neurons may involve both transcriptional and post-transcriptional mechanisms including a decreased degradation of the protein through proteasomal or autophagic processes...
November 28, 2017: Current Neuropharmacology
https://www.readbyqxmd.com/read/29183391/oxidative-stress-and-cellular-pathologies-in-parkinson-s-disease
#20
REVIEW
Lesly Puspita, Sun Young Chung, Jae-Won Shim
Parkinson's disease (PD) is a chronic and progressive neurodegeneration of dopamine neurons in the substantia nigra. The reason for the death of these neurons is unclear; however, studies have demonstrated the potential involvement of mitochondria, endoplasmic reticulum, α-synuclein or dopamine levels in contributing to cellular oxidative stress as well as PD symptoms. Even though those papers had separately described the individual roles of each element leading to neurodegeneration, recent publications suggest that neurodegeneration is the product of various cellular interactions...
November 28, 2017: Molecular Brain
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