keyword
MENU ▼
Read by QxMD icon Read
search

parkinson's disease and mitochondria

keyword
https://www.readbyqxmd.com/read/27906179/pink1-dependent-phosphorylation-of-pink1-and-parkin-is-essential-for-mitochondrial-quality-control
#1
Na Zhuang, Lin Li, She Chen, Tao Wang
Mitochondrial dysfunction has been linked to the pathogenesis of a large number of inherited diseases in humans, including Parkinson's disease, the second most common neurodegenerative disorder. The Parkinson's disease genes pink1 and parkin, which encode a mitochondrially targeted protein kinase, and an E3 ubiquitin ligase, respectively, participate in a key mitochondrial quality-control pathway that eliminates damaged mitochondria. In the current study, we established an in vivo PINK1/Parkin-induced photoreceptor neuron degeneration model in Drosophila with the aim of dissecting the PINK1/Parkin pathway in detail...
December 1, 2016: Cell Death & Disease
https://www.readbyqxmd.com/read/27884192/role-of-cytochrome-c-in-%C3%AE-synuclein-radical-formation-implications-of-%C3%AE-synuclein-in-neuronal-death-in-maneb-and-paraquat-induced-model-of-parkinson-s-disease
#2
Ashutosh Kumar, Douglas Ganini, Ronald P Mason
BACKGROUND: The pathological features of Parkinson's disease (PD) include an abnormal accumulation of α-synuclein in the surviving dopaminergic neurons. Though PD is multifactorial, several epidemiological reports show an increased incidence of PD with co-exposure to pesticides such as Maneb and paraquat (MP). In pesticide-related PD, mitochondrial dysfunction and α-synuclein oligomers have been strongly implicated, but the link between the two has not yet been understood. Similarly, the biological effects of α-synuclein or its radical chemistry in PD is largely unknown...
November 24, 2016: Molecular Neurodegeneration
https://www.readbyqxmd.com/read/27881168/loss-of-porin-function-in-dopaminergic-neurons-of-drosophila-is-suppressed-by-buffy
#3
P Githure M'Angale, Brian E Staveley
BACKGROUND: Mitochondrial porin, also known as the voltage-dependent anion channel (VDAC), is a multi-functional channel protein that shuttles metabolites between the mitochondria and the cytosol and implicated in cellular life and death decisions. The inhibition of porin under the control of neuronal Ddc-Gal4 result in short lifespan and in an age-dependent loss in locomotor function, phenotypes that are strongly associated with Drosophila models of Parkinson disease. METHODS: Loss of porin function was achieved through exploitation of RNA interference while derivative lines were generated by homologous recombination and tested by PCR...
November 24, 2016: Journal of Biomedical Science
https://www.readbyqxmd.com/read/27879341/title-dynamin-functions-and-ligands-classical-mechanism-behind
#4
Mahaveer Singh, Hemant Jadhav, Tanya B
Dynamin is a GTPase, which plays a vital role in clathrin dependent endocytosis and other vesicular trafficking processes. Dynamin acts as scissor with debatable mechanism for newly formed vesicles originating from plasma membrane. Dynamin related proteins are important components in scission of various organelles such as clathrin coated vesicles, phagosomes and mitochondria, etc. helping in organelle division, viral resistance and mitochondrial fusion/division. Dysfunction and mutations in dynamin have been implicated in various disorders, where endocytic trafficking is involved, such as Alzheimer's, Parkinson's, Huntington's, Charcot-Marie Tooth disease, Heart failure, Schizophrenia, Epilepsy, Cancer, Optic atrophy, Down syndrome, Osteoporosis etc...
November 22, 2016: Molecular Pharmacology
https://www.readbyqxmd.com/read/27873462/mitochondrial-dysfunction-and-biogenesis-in-neurodegenerative-diseases-pathogenesis-and-treatment
#5
REVIEW
Mojtaba Golpich, Elham Amini, Zahurin Mohamed, Raymond Azman Ali, Norlinah Mohamed Ibrahim, Abolhassan Ahmadiani
Neurodegenerative diseases are a heterogeneous group of disorders that are incurable and characterized by the progressive degeneration of the function and structure of the central nervous system (CNS) for reasons that are not yet understood. Neurodegeneration is the umbrella term for the progressive death of nerve cells and loss of brain tissue. Because of their high energy requirements, neurons are especially vulnerable to injury and death from dysfunctional mitochondria. Widespread damage to mitochondria causes cells to die because they can no longer produce enough energy...
November 22, 2016: CNS Neuroscience & Therapeutics
https://www.readbyqxmd.com/read/27872751/novel-gene-tmem230-linked-to-parkinson-s-disease
#6
EDITORIAL
Diana A Olszewska, Conor Fearon, Tim Lynch
Mutations in six genes are known to cause Parkinson's disease (PD) (autosomal dominant: alpha-synuclein, LRRK2, VPS35 and autosomal recessive: Parkin, PINK1 and DJ1) and number of other genes are implicated. In a recent article Deng and colleagues studied a large four generation American family of European descent and linked mutations in a novel gene, transmembrane-protein 230 gene (TMEM230) with lewy body confirmed PD. The authors demonstrated that pathogenic TMEM230 variants in primary mouse neurons affected movement of synaptic vesicles suggesting that TMEM230 may slow vesicular transport...
2016: Journal of Clinical Movement Disorders
https://www.readbyqxmd.com/read/27866262/impairment-of-mitochondria-dynamics-by-human-a53t-%C3%AE-synuclein-and-rescue-by-nap-davunetide-in-a-cell-model-for-parkinson-s-disease
#7
T Q Melo, K C van Zomeren, M F R Ferrari, H W G M Boddeke, J C V M Copray
The formation of oligomers and aggregates of overexpressed or mutant α-synuclein play a role in the degeneration of dopaminergic neurons in Parkinson's disease by causing dysfunction of mitochondria, reflected in their disturbed mobility and production of ROS. The mode of action and mechanisms underlying this mitochondrial impairment is still unclear. We have induced stable expression of wild-type, A30P or A53T α-synuclein in neuronally differentiated SH-SY5Y neuroblastoma cells and studied anterograde and retrograde mitochondrial trafficking in this cell model for Parkinson's disease...
November 19, 2016: Experimental Brain Research. Experimentelle Hirnforschung. Expérimentation Cérébrale
https://www.readbyqxmd.com/read/27830778/defects-in-trafficking-bridge-parkinson-s-disease-pathology-and-genetics
#8
Asa Abeliovich, Aaron D Gitler
Parkinson's disease is a debilitating, age-associated movement disorder. A central aspect of the pathophysiology of Parkinson's disease is the progressive demise of midbrain dopamine neurons and their axonal projections, but the underlying causes of this loss are unclear. Advances in genetics and experimental model systems have illuminated an important role for defects in intracellular transport pathways to lysosomes. The accumulation of altered proteins and damaged mitochondria, particularly at axon terminals, ultimately might overwhelm the capacity of intracellular disposal mechanisms...
November 9, 2016: Nature
https://www.readbyqxmd.com/read/27830583/dynamin-related-protein-1-drp1-mediating-mitophagy-contributes-to-the-pathophysiology-of-nervous-system-diseases-and-brain-injury
#9
REVIEW
Qiong Wu, Cheng-Liang Luo, Lu-Yang Tao
As the main source of energy (celluar ATP) in eukaryotic cells, mitochondria are involved in cellular physiology and pathology. The balance of mitochondrial dynamic, fission and fusion regulated by quality control mechanisms, provides a guarantee for maintaining mitochondrial function, even celluar function. Worn out mitochondria would be removed through mitophagy which is regulated by autophagy related proteins and mitochondrial membrane proteins. Drp1, dynamic-related protein 1, is regarded as one of the most important proteins to evaluate mitochondrial fission mediating mitophagy in neurodegenerative diseases (eg...
November 10, 2016: Histology and Histopathology
https://www.readbyqxmd.com/read/27814651/mitochondria-in-the-pathophysiology-of-alzheimer-s-and-parkinson-s-diseases
#10
Isaac G Onyango, Shaharyar M Khan, James P Bennett
Mitochondria are responsible for the majority of energy production in energy-intensive tissues like brain, modulate Ca(+2) signaling and control initiation of cell death. Because of their extensive use of oxygen and lack of protective histone proteins, mitochondria are vulnerable to oxidative stress (ROS)-induced damage to their genome (mtDNA), respiratory chain proteins and ROS repair enzymes. Animal and cell models of PD use toxins that impair mitochondrial complex I activity. Maintenance of mitochondrial mass, mitochondrial biogenesis (mitobiogenesis), particularly in high-energy brain, occurs through complex signaling pathways involving the upstream "master regulator" PGC-1alpha that is transcriptionally and post-translationally regulated...
January 1, 2017: Frontiers in Bioscience (Landmark Edition)
https://www.readbyqxmd.com/read/27809706/oxidative-stress-and-mitochondrial-dysfunction-linked-neurodegenerative-disorders
#11
Md Torequl Islam
Reactive species play an important role in physiological functions. Overproduction of reactive species, notably reactive oxygen (ROS) and nitrogen (RNS) species along with the failure of balance by the body's antioxidant enzyme systems results in destruction of cellular structures, lipids, proteins, and genetic materials such as DNA and RNA. Moreover, the effects of reactive species on mitochondria and their metabolic processes eventually cause a rise in ROS/RNS levels, leading to oxidation of mitochondrial proteins, lipids, and DNA...
November 3, 2016: Neurological Research
https://www.readbyqxmd.com/read/27806193/neuroprotective-effect-of-a-new-7-8-dihydroxycoumarin-based-fe2-cu2-chelator-in-cell-and-animal-models-of-parkinson-s-disease
#12
Pabla Aguirre, Olimpo García-Beltrán, Victoria Tapia, Yorka Muñoz, Bruce Kennedy Cassels, Marco T Nunez
Disturbed iron homeostasis, often coupled to mitochondrial dysfunction, plays an important role in the progression of common neurodegenerative diseases such as Parkinson disease (PD). Recent studies have underlined the relevance of iron chelation therapy for the treatment of these diseases. Here we describe the synthesis, chemical and biological characterization of the multifunctional chelator 7,8-dihydroxy-4-((methylamino)methyl)-2H-chromen-2-one (DHC12). Metal selectivity of DHC12 was Cu2+ ̴ Fe2+ > Zn2+ > Fe3+...
November 2, 2016: ACS Chemical Neuroscience
https://www.readbyqxmd.com/read/27778029/-advances-in-the-association-of-atp-sensitive-potassium-channels-and-parkinson-s-disease
#13
Xi-Xun DU, Kang Qin, Qian Jiao, Jun-Xia Xie, Hong Jiang
ATP-sensitive potassium channels (KATP), as an inward rectifying potassium channel, are widely distributed in many types of tissues. KATP are activated by the depletion of ATP level and the increase in oxidative stress in cells. The activity of KATP couples cell metabolism with electrical activity and results in membrane hyperpolarization. KATP are ubiquitously distributed in the brain, including substantia nigra, hippocampus, hypothalamus, cerebral cortex, dorsal nucleus of vagus and glial cells, and participate in neuronal excitability, mitochondria homeostasis and neurotransmitter release...
October 25, 2016: Sheng Li Xue Bao: [Acta Physiologica Sinica]
https://www.readbyqxmd.com/read/27771430/neuronal-protection-against-oxidative-insult-by-polyanhydride-nanoparticle-based-mitochondria-targeted-antioxidant-therapy
#14
Timothy M Brenza, Shivani Ghaisas, Julia E Vela Ramirez, Dilshan Harischandra, Vellareddy Anantharam, Balaraman Kalyanaraman, Anumantha G Kanthasamy, Balaji Narasimhan
A progressive loss of neuronal structure and function is a signature of many neurodegenerative conditions including chronic traumatic encephalopathy, Parkinson's, Huntington's and Alzheimer's diseases. Mitochondrial dysfunction and oxidative and nitrative stress have been implicated as key pathological mechanisms underlying the neurodegenerative processes. However, current therapeutic approaches targeting oxidative damage are ineffective in preventing the progression of neurodegeneration. Mitochondria-targeted antioxidants were recently shown to alleviate oxidative damage...
October 19, 2016: Nanomedicine: Nanotechnology, Biology, and Medicine
https://www.readbyqxmd.com/read/27761515/swath-ms-proteome-profiling-data-comparison-of-dj-1-parkin-and-pink1-knockout-rat-striatal-mitochondria
#15
Kelly L Stauch, Lance M Villeneuve, Phillip R Purnell, Sanjit Pandey, Chittibabu Guda, Howard S Fox
This article reports changes in the striatal non-synaptic mitochondrial proteome of DJ-1, Parkin, and PINK1 knockout (KO) rats at 3 months of age. DJ-1, Parkin, and PINK1 mutations cause autosomal-recessive parkinsonism. It is thought that loss of function of these proteins contributes to the onset and pathogenesis of Parkinson׳s disease (PD). As DJ-1, Parkin, and PINK1 have functions in the regulation of mitochondria, the dataset generated here highlights protein expression changes, which can be helpful for understanding pathological mitochondrial alterations...
December 2016: Data in Brief
https://www.readbyqxmd.com/read/27738100/novel-compounds-targeting-the-mitochondrial-protein-vdac1-inhibit-apoptosis-and-protect-against-mitochondrial-dysfunction
#16
Danya Ben-Hail, Racheli Begas-Shvartz, Moran Shalev, Anna Shteinfer-Kuzmine, Arie Gruzman, Simona Reina, Vito De Pinto, Varda Shoshan-Barmatz
Apoptosis is thought to play a critical role in several pathological processes, such as neurodegenerative diseases (i.e. Parkinson's and Alzheimer's diseases) and various cardiovascular diseases. Despite the fact that apoptotic mechanisms are well defined, there is still no substantial therapeutic strategy to stop or even slow this process. Thus, there is an unmet need for therapeutic agents that are able to block or slow apoptosis in neurodegenerative and cardiovascular diseases. The outer mitochondrial membrane protein voltage-dependent anion channel 1 (VDAC1) is a convergence point for a variety of cell survival and death signals, including apoptosis...
November 25, 2016: Journal of Biological Chemistry
https://www.readbyqxmd.com/read/27733642/mitochondrial-dependent-mechanisms-are-involved-in-angiotensin-ii-induced-apoptosis-in-dopaminergic-neurons
#17
Zhou Ou, Teng Jiang, Qing Gao, You-Yong Tian, Jun-Shan Zhou, Liang Wu, Jian-Quan Shi, Ying-Dong Zhang
INTRODUCTION: We recently demonstrated that angiotensin II (Ang II) was involved in the etiology of Parkinson's disease (PD) via induction of apoptosis of dopaminergic neurons, but the mechanisms are not completely elucidated. Here, we asked whether mitochondrial-dependent mechanisms contributed to the Ang II-induced dopaminergic neuronal apoptosis. MATERIALS AND METHODS: CATH.a cells were incubated with Ang II in combination with mitochondrial permeability transition pore (mPTP) inhibitors or angiotensin receptor antagonists, and apoptosis rate, caspase-3 activity, cytochrome c levels, and mPTP opening were assessed...
October 2016: Journal of the Renin-angiotensin-aldosterone System: JRAAS
https://www.readbyqxmd.com/read/27733604/monomeric-alpha-synuclein-exerts-a-physiological-role-on-brain-atp-synthase
#18
Marthe H R Ludtmann, Plamena R Angelova, Natalia N Ninkina, Sonia Gandhi, Vladimir L Buchman, Andrey Y Abramov
: Misfolded α-synuclein is a key factor in the pathogenesis of Parkinson's disease (PD). However, knowledge about a physiological role for the native, unfolded α-synuclein is limited. Using brains of mice lacking α-, β-, and γ-synuclein, we report that extracellular monomeric α-synuclein enters neurons and localizes to mitochondria, interacts with ATP synthase subunit α, and modulates ATP synthase function. Using a combination of biochemical, live-cell imaging and mitochondrial respiration analysis, we found that brain mitochondria of α-, β-, and γ-synuclein knock-out mice are uncoupled, as characterized by increased mitochondrial respiration and reduced mitochondrial membrane potential...
October 12, 2016: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/27714635/mitochondria-associated-membranes-mams-overview-and-its-role-in-parkinson-s-disease
#19
M Rodríguez-Arribas, S M S Yakhine-Diop, J M Bravo-San Pedro, P Gómez-Suaga, R Gómez-Sánchez, G Martínez-Chacón, J M Fuentes, R A González-Polo, M Niso-Santano
Mitochondria-associated membranes (MAMs) are structures that regulate physiological functions between endoplasmic reticulum (ER) and mitochondria in order to maintain calcium signaling and mitochondrial biogenesis. Several proteins located in MAMs, including those encoded by PARK genes and some of neurodegeneration-related proteins (huntingtin, presenilin, etc.), ensure this regulation. In this regard, MAM alteration is associated with neurodegenerative diseases such as Parkinson's (PD), Alzheimer's (AD), and Huntington's diseases (HD) and contributes to the appearance of the pathogenesis features, i...
October 6, 2016: Molecular Neurobiology
https://www.readbyqxmd.com/read/27703082/fluorescent-parkin-cell-based-assay-development-for-the-screening-of-drugs-against-parkinson-disease
#20
Patricia Villacé, Rosa M Mella, Meritxell Roura-Ferrer, María Valcárcel, Clarisa Salado, Amaia Castilla, Danel Kortazar
Parkinson disease (PD) is a prevalent neurodegenerative disease characterized by selective degeneration of dopaminergic neurons in the substantia nigra, causing tremor and motor impairment. Parkin protein, whose mutants are the cause of Parkinson disease type 2 (PARK2), has been mechanistically linked to the regulation of apoptosis and the turnover of damaged mitochondria. Several studies have implicated aberrant mitochondria as a key contributor to the development of PD. In the attempt to discover new drugs, high-content cell-based assays are becoming more important to mimic the nature of biological processes and their diversifications in diseases and will be essential for lead identification and the optimization of therapeutic candidates...
October 4, 2016: Journal of Biomolecular Screening
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"