keyword
MENU ▼
Read by QxMD icon Read
search

parkinson's disease and mitochondria

keyword
https://www.readbyqxmd.com/read/29755410/mitochondrial-chaperones-in-the-brain-safeguarding-brain-health-and-metabolism
#1
José Pedro Castro, Kristina Wardelmann, Tilman Grune, André Kleinridders
The brain orchestrates organ function and regulates whole body metabolism by the concerted action of neurons and glia cells in the central nervous system. To do so, the brain has tremendously high energy consumption and relies mainly on glucose utilization and mitochondrial function in order to exert its function. As a consequence of high rate metabolism, mitochondria in the brain accumulate errors over time, such as mitochondrial DNA (mtDNA) mutations, reactive oxygen species, and misfolded and aggregated proteins...
2018: Frontiers in Endocrinology
https://www.readbyqxmd.com/read/29755319/ambra1-mediated-mitophagy-counteracts-oxidative-stress-and-apoptosis-induced-by-neurotoxicity-in-human-neuroblastoma-sh-sy5y-cells
#2
Anthea Di Rita, Pasquale D'Acunzo, Luca Simula, Silvia Campello, Flavie Strappazzon, Francesco Cecconi
Therapeutic strategies are needed to protect dopaminergic neurons in Parkinson's disease (PD) patients. Oxidative stress caused by dopamine may play an important role in PD pathogenesis. Selective autophagy of mitochondria (mitophagy), mainly regulated by PINK1 and PARKIN, plays an important role in the maintenance of cell homeostasis. Mutations in those genes cause accumulation of damaged mitochondria, leading to nigral degeneration and early-onset PD. AMBRA1ActA is a fusion protein specifically expressed at the mitochondria, and whose expression has been shown to induce a powerful mitophagy in mammalian cells...
2018: Frontiers in Cellular Neuroscience
https://www.readbyqxmd.com/read/29751692/brain-mitochondria-aging-and-parkinson-s-disease
#3
REVIEW
Mario Rango, Nereo Bresolin
This paper reconsiders the role of mitochondria in aging and in Parkinson's Disease (PD). The most important risk factor for PD is aging. Alterations in mitochondrial activity are typical of aging. Mitochondrial aging is characterized by decreased oxidative phosphorylation, proteasome activity decrease, altered autophagy, and mitochondrial dysfunction. Beyond declined oxidative phosphorylation, mitochondrial dysfunction consists of a decline of beta-oxidation as well as of the Krebs cycle. Not inherited mitochondrial DNA (mtDNA) mutations are acquired over time and parallel the decrease in oxidative phosphorylation...
May 11, 2018: Genes
https://www.readbyqxmd.com/read/29748634/gene-by-environment-interactions-that-disrupt-mitochondrial-homeostasis-cause-neurodegeneration-in-c-elegans-parkinson-s-models
#4
Hanna Kim, Rylee J Perentis, Guy A Caldwell, Kim A Caldwell
Parkinson's disease (PD) is a complex multifactorial disorder where environmental factors interact with genetic susceptibility. Accumulating evidence suggests that mitochondria have a central role in the progression of neurodegeneration in sporadic and/or genetic forms of PD. We previously reported that exposure to a secondary metabolite from the soil bacterium, Streptomyces venezuelae, results in age- and dose-dependent dopaminergic (DA) neurodegeneration in Caenorhabditis elegans and human SH-SY5Y neurons...
May 10, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/29740311/-sophora-flavescens-aiton-decreases-mpp-induced-mitochondrial-dysfunction-in-sh-sy5y-cells
#5
Hee-Young Kim, Hyongjun Jeon, Hyungwoo Kim, Sungtae Koo, Seungtae Kim
Sophora flavescens Aiton (SF) has been used to treat various diseases including fever and inflammation in China, South Korea and Japan. Several recent reports have shown that SF has anti-inflammatory and anti-apoptotic effects, indicating that it is a promising candidate for treatment of Parkinson's disease (PD). We evaluated the protective effect of SF against neurotoxin 1-methyl-4-phenylpyridinium ion (MPP+ )-induced mitochondrial dysfunction in SH-SY5Y human neuroblastoma cells, an in vitro PD model. SH-SY5Y cells were incubated with SF for 24 h, after which they were treated with MPP+ ...
2018: Frontiers in Aging Neuroscience
https://www.readbyqxmd.com/read/29729423/interaction-between-a-mapt-variant-causing-frontotemporal-dementia-and-mutant-app-affects-axonal-transport
#6
Robert Adalbert, Stefan Milde, Claire Durrant, Kunie Ando, Virginie Stygelbout, Zehra Yilmaz, Stacey Gould, Jean-Pierre Brion, Michael P Coleman
In Alzheimer's disease, many indicators point to a central role for poor axonal transport, but the potential for stimulating axonal transport to alleviate the disease remains largely untested. Previously, we reported enhanced anterograde axonal transport of mitochondria in 8- to 11-month-old MAPTP301L knockin mice, a genetic model of frontotemporal dementia with parkinsonism-17T. In this study, we further characterized the axonal transport of mitochondria in younger MAPTP301L mice crossed with the familial Alzheimer's disease model, TgCRND8, aiming to test whether boosting axonal transport in young TgCRND8 mice can alleviate axonal swelling...
April 5, 2018: Neurobiology of Aging
https://www.readbyqxmd.com/read/29718367/increased-oxidative-stress-exacerbates-%C3%AE-synuclein-aggregation-in-vivo
#7
Owen Scudamore, Thomas Ciossek
Increasing evidence suggests a relationship between oxidative stress and α-synuclein aggregation, the primary pathological hallmark of Parkinson disease (PD). However, a direct causal relationship has not yet been established in vivo in mouse models of PD. Superoxide dismutase 2 (SOD2) is rate limiting in the antioxidant machinery of the mitochondria and even its partial deficiency elevates oxidative stress in mice. Therefore, in order to investigate a possible interaction between oxidative stress and α-synuclein aggregation in vivo, a transgenic model of PD with haplodeficiency for SOD2 was generated on the basis of the well-characterized murine (Thy-1)-h[A30P]-α-synuclein transgenic line...
April 27, 2018: Journal of Neuropathology and Experimental Neurology
https://www.readbyqxmd.com/read/29704589/mitochondrial-alterations-in-parkinson-s-disease-human-samples-and-cellular-models
#8
Mara Zilocchi, Giovanna Finzi, Marta Lualdi, Fausto Sessa, Mauro Fasano, Tiziana Alberio
Mitochondrial impairment is one of the most important hallmarks of Parkinson's disease (PD) pathogenesis. In this work, we wanted to verify the molecular basis of altered mitochondrial dynamics and disposal in Substantia nigra specimens of sporadic PD patients, by the comparison with two cellular models of PD. Indeed, SH-SY5Y cells were treated with either dopamine or 1-methyl-4-phenylpyridinium (MPP+ ) in order to highlight the effect of altered dopamine homeostasis and of complex I inhibition, respectively...
April 25, 2018: Neurochemistry International
https://www.readbyqxmd.com/read/29702063/mitochondrial-interaction-of-alpha-synuclein-leads-to-irreversible-translocation-and-complex-i-impairment
#9
Jimena H Martínez, Federico Fuentes, Virginia Vanasco, Silvia Alvarez, Agustina Alaimo, Adriana Cassina, Federico Coluccio Leskow, Francisco Velazquez
α-synuclein is involved in both familial and sporadic Parkinson's disease. Although its interaction with mitochondria has been well documented several aspects remains unknown or under debate; such as the specific sub-mitochondrial localization of α-synuclein or the dynamics of the interaction. It has been suggested that α-synuclein could only interact with ER-associated mitochondria. Variety of model systems and experimental conditions makes difficult to compare results and extract definitive conclusions...
April 24, 2018: Archives of Biochemistry and Biophysics
https://www.readbyqxmd.com/read/29688484/effect-of-the-catechol-o-methyltransferase-inhibitors-tolcapone-and-entacapone-on-fatty-acid-metabolism-in-heparg-cells
#10
David Grünig, Andrea Felser, Urs Duthaler, Jamal Bouitbir, Stephan Krähenbühl
Tolcapone and entacapone are catechol-O-methyltransferase (COMT) inhibitors used in patients with Parkinson's disease. For tolcapone, patients with liver failure have been reported with microvesicular steatosis observed in the liver biopsy of one patient. We therefore investigated the impact of tolcapone and entacapone on fatty acid metabolism in HepaRG cells exposed for 24 hours and on acutely exposed mouse liver mitochondria. In HepaRG cells, tolcapone induced lipid accumulation starting at 100µM, whereas entacapone was ineffective up to 200µM...
April 23, 2018: Toxicological Sciences: An Official Journal of the Society of Toxicology
https://www.readbyqxmd.com/read/29683090/effects-of-aging-in-the-striatum-and-substantia-nigra-of-a-parkinson-s-disease-animal-model
#11
Rodrigo Portes Ureshino, Angelica Jardim Costa, Adolfo Garcia Erustes, Gustavo José da Silva Pereira, Rita Sinigaglia-Coimbra, Soraya Soubhi Smaili
Aging is a multifactorial process associated with functional deficits, and the brain is more prone to developing chronic degenerative diseases such as Parkinson's disease. Several groups have tried to correlate the age-related ultrastructural alterations to the neurodegeneration process using in vivo pharmacological models, but due to the limitations of the animal models, particularly in aged animals, the results are difficult to interpret. In this work, we investigated neurodegeneration induced by rotenone, as a pharmacological model of Parkinson's disease, in both young and aged Wistar rats...
April 2018: Toxicologic Pathology
https://www.readbyqxmd.com/read/29682760/protective-role-of-parkin-in-skeletal-muscle-contractile-and-mitochondrial-function
#12
Gilles Gouspillou, Richard Godin, Jérome Piquereau, Martin Picard, Mahroo Mofarrahi, Jasmin Mathew, Fennigje M Purves-Smith, Nicolas Sgarioto, Russell T Hepple, Yan Burelle, Sabah Na Hussain
KEY POINTS SUMMARY: Parkin, an E3 ubiquitin ligase encoded by the Park2 gene, has been implicated in the regulation of mitophagy, a quality control process whereby defective mitochondria are degraded. The exact physiological significance of Parkin in regulating mitochondrial function and contractility in skeletal muscle remains largely unexplored. Using Park2-/- mice, we show that Parkin ablation causes a decrease in muscle specific force, a severe decrease in mitochondrial respiration, mitochondrial uncoupling and an increased susceptibility to opening of the permeability transition pore...
April 22, 2018: Journal of Physiology
https://www.readbyqxmd.com/read/29626647/multiple-pathways-for-mitophagy-a-neurodegenerative-conundrum-for-parkinson-s-disease
#13
REVIEW
Charleen T Chu
It has been nearly a decade since the first landmark studies implicating familial recessive Parkinson's disease genes in the regulation of selective mitochondrial autophagy. The PTEN-induced kinase 1 (PINK1) and the E3 ubiquitin ligase Parkin (encoded by the PARK2 gene) act together to mark depolarized mitochondria for degradation. There is now an extensive body of literature detailing key mediators and steps in this pathway, based mostly on work in transformed cell lines. However, the degree to which PINK1-triggered mitophagy contributes to mitochondrial quality control in the mammalian brain, and the extent to which its disruption contributes to Parkinson's disease pathogenesis remain uncertain...
April 4, 2018: Neuroscience Letters
https://www.readbyqxmd.com/read/29624777/de-novo-tetrahydrobiopterin-biosynthesis-is-impaired-in-the-inflammed-striatum-of-parkin-mice
#14
Roberta de Paula Martins, Viviane Glaser, Aderbal S Aguiar, Priscila Maximiliano de Paula Ferreira, Karina Ghisoni, Débora da Luz Scheffer, Laurence Lanfumey, Rita Raisman-Vozari, Olga Corti, Ana Lucia De Paul, Rodrigo Augusto da Silva, Alexandra Latini
Parkinson's disease (PD), the second-most prevalent neurodegenerative disease, is primarily characterized by neurodegeneration in the substantia nigra pars compacta, resulting in motor impairment. Loss-of-function mutations in parkin are the major cause of the early-onset familial form of the disease. Although rodents deficient in parkin (parkin(-/-)) have some dopaminergic system dysfunction associated with central oxidative stress and energy metabolism deficiencies, these animals only display nigrostriatal pathway degeneration under inflammatory conditions...
April 6, 2018: Cell Biology International
https://www.readbyqxmd.com/read/29619740/nicotine-modulates-mitochondrial-dynamics-in-hippocampal-neurons
#15
Juan A Godoy, Angel G Valdivieso, Nibaldo C Inestrosa
Mitochondria are widely recognized as fundamental organelles for cellular physiology and constitute the main energy source for different cellular processes. The location, morphology, and interactions of mitochondria with other organelles, such as the endoplasmic reticulum (ER), have emerged as critical events capable of determining cellular fate. Mitochondria-related functions have proven particularly relevant in neurons; mitochondria are necessary for proper neuronal morphogenesis and the highly energy-demanding synaptic transmission process...
April 4, 2018: Molecular Neurobiology
https://www.readbyqxmd.com/read/29616350/mitochondrial-dysfunction-in-parkinson-s-disease-new-mechanistic-insights-and-therapeutic-perspectives
#16
REVIEW
Jin-Sung Park, Ryan L Davis, Carolyn M Sue
PURPOSE OF REVIEW: Parkinson's disease (PD) is a complex neurodegenerative disorder, the aetiology of which is still largely unknown. Overwhelming evidence indicates that mitochondrial dysfunction is a central factor in PD pathophysiology. Here we review recent developments around mitochondrial dysfunction in familial and sporadic PD, with a brief overview of emerging therapies targeting mitochondrial dysfunction. RECENT FINDINGS: Increasing evidence supports the critical role for mitochondrial dysfunction in the development of sporadic PD, while the involvement of familial PD-related genes in the regulation of mitochondrial biology has been expanded by the discovery of new mitochondria-associated disease loci and the identification of their novel functions...
April 3, 2018: Current Neurology and Neuroscience Reports
https://www.readbyqxmd.com/read/29604226/stem-cell-modeling-of-mitochondrial-parkinsonism-reveals-key-functions-of-opa1
#17
Mindaugas Jonikas, Martin Madill, Alexandre Mathy, Theresa Zekoll, Christos E Zois, Simon Wigfield, Marzena Kurzawa-Akanbi, Cathy Browne, David Sims, Patrick F Chinnery, Sally A Cowley, George K Tofaris
OBJECTIVE: Defective mitochondrial function due to OPA1 mutations causes primarily optic atrophy and less commonly neurodegenerative syndromes. The pathomechanism by which OPA1 mutations trigger diffuse loss of neurons in some but not all patients is unknown. Here we used a tractable iPSC-based model to capture the biology of OPA1 haploinsufficiency in cases presenting with classic eye disease versus syndromic parkinsonism. METHODS: iPSC were generated from two patients with OPA1 haploinsufficiency and two controls and differentiated into dopaminergic neurons...
March 31, 2018: Annals of Neurology
https://www.readbyqxmd.com/read/29599708/distinct-mechanisms-of-pathogenic-dj-1-mutations-in-mitochondrial-quality-control
#18
Daniela Strobbe, Alexis A Robinson, Kirsten Harvey, Lara Rossi, Caterina Ferraina, Valerio de Biase, Carlo Rodolfo, Robert J Harvey, Michelangelo Campanella
The deglycase and chaperone protein DJ-1 is pivotal for cellular oxidative stress responses and mitochondrial quality control. Mutations in PARK7 , encoding DJ-1, are associated with early-onset familial Parkinson's disease and lead to pathological oxidative stress and/or disrupted protein degradation by the proteasome. The aim of this study was to gain insights into the pathogenic mechanisms of selected DJ-1 missense mutations, by characterizing protein-protein interactions, core parameters of mitochondrial function, quality control regulation via autophagy, and cellular death following dopamine accumulation...
2018: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/29588162/aminochrome-decreases-ngf-gdnf-and-induces-neuroinflammation-in-organotypic-midbrain-slice-cultures
#19
Fillipe M de Araújo, Rafael S Ferreira, Cleide S Souza, Cleonice Creusa Dos Santos, Tácio L R S Rodrigues, Juliana Helena C E Silva, Juciano Gasparotto, Daniel Pens Gelain, Ramon S El-Bachá, Maria de Fátima D Costa, José Claudio M Fonseca, Juan Segura-Aguilar, Silvia L Costa, Victor Diogenes A Silva
Recent evidence shows that aminochrome induces glial activation related to neuroinflammation. This dopamine derived molecule induces formation and stabilization of alpha-synuclein oligomers, mitochondria dysfunction, oxidative stress, dysfunction of proteasomal and lysosomal systems, endoplasmic reticulum stress and disruption of the microtubule network, but until now there has been no evidence of effects on production of cytokines and neurotrophic factors, that are mechanisms involved in neuronal loss in Parkinson's disease (PD)...
March 24, 2018: Neurotoxicology
https://www.readbyqxmd.com/read/29581821/unraveling-the-burden-of-iron-in-neurodegeneration-intersections-with-amyloid-beta-peptide-pathology
#20
REVIEW
Romina María Uranga, Gabriela Alejandra Salvador
Iron overload is a hallmark of many neurodegenerative processes such as Alzheimer's, Parkinson's, and Huntington's diseases. Unbound iron accumulated as a consequence of brain aging is highly reactive with water and oxygen and produces reactive oxygen species (ROS) or free radicals. ROS are toxic compounds able to damage cell membranes, DNA, and mitochondria. Which are the mechanisms involved in neuronal iron homeostasis and in neuronal response to iron-induced oxidative stress constitutes a cutting-edge topic in metalloneurobiology...
2018: Oxidative Medicine and Cellular Longevity
keyword
keyword
85731
1
2
Fetch more papers »
Fetching more papers... Fetching...
Read by QxMD. Sign in or create an account to discover new knowledge that matter to you.
Remove bar
Read by QxMD icon Read
×

Search Tips

Use Boolean operators: AND/OR

diabetic AND foot
diabetes OR diabetic

Exclude a word using the 'minus' sign

Virchow -triad

Use Parentheses

water AND (cup OR glass)

Add an asterisk (*) at end of a word to include word stems

Neuro* will search for Neurology, Neuroscientist, Neurological, and so on

Use quotes to search for an exact phrase

"primary prevention of cancer"
(heart or cardiac or cardio*) AND arrest -"American Heart Association"