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https://www.readbyqxmd.com/read/29767788/acute-maneb-exposure-significantly-alters-both-glycolysis-and-mitochondrial-function-in-neuroblastoma-cells
#1
Colin C Anderson, Stefanos Aivazidis, Crystal L Kuzyk, Abhilasha Jain, James R Roede
The pesticides paraquat (PQ) and maneb (MB) have been described as environmental risk factors for Parkinson's disease (PD), with mechanisms associated with mitochondrial dysfunction and reactive oxygen species (ROS) generation. A combined exposure of PQ and MB in murine models and neuroblastoma cells has been utilized to further advance understanding of the PD phenotype. MB acts as a redox modulator through alkylation of protein thiols and has been previously characterized to inhibit complex III of the electron transport chain (ETC) and uncouple the mitochondrial proton gradient...
May 14, 2018: Toxicological Sciences: An Official Journal of the Society of Toxicology
https://www.readbyqxmd.com/read/29759145/thymoquinone-increases-the-expression-of-neuroprotective-proteins-while-decreasing-the-expression-of-pro-inflammatory-cytokines-and-the-gene-expression-nf%C3%AE%C2%BAb-pathway-signaling-targets-in-lps-ifn%C3%AE-activated-bv-2-microglia-cells
#2
Makini K Cobourne-Duval, Equar Taka, Patricia Mendonca, Karam F A Soliman
Neuroinflammation and microglial activation are pathological markers of a number of central nervous system (CNS) diseases. Chronic activation of microglia induces the release of excessive amounts of reactive oxygen species (ROS) and pro-inflammatory cytokines. Additionally, chronic microglial activation has been implicated in several neurodegenerative diseases, including Alzheimer's disease and Parkinson's disease. Thymoquinone (TQ) has been identified as one of the major active components of the natural product Nigella sativa seed oil...
July 15, 2018: Journal of Neuroimmunology
https://www.readbyqxmd.com/read/29755410/mitochondrial-chaperones-in-the-brain-safeguarding-brain-health-and-metabolism
#3
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/29755339/therapeutic-potential-of-a-prolyl-hydroxylase-inhibitor-fg-4592-for-parkinson-s-diseases-in-vitro-and-in-vivo-regulation-of-redox-biology-and-mitochondrial-function
#4
Xuan Li, Xin-Xin Cui, Ya-Jing Chen, Ting-Ting Wu, Huaxi Xu, Huiyong Yin, Yun-Cheng Wu
As the main transcription factor that regulates the cellular responses to hypoxia, Hypoxia-inducible factor-1α (HIF-1α) plays an important role in the pathogenesis of Parkinson's disease (PD). HIF-1α is normally degraded through ubiquitination after hydroxylation by prolyl hydroxylases (PHD). Emerging evidence has suggested that HIF PHD inhibitors (HIF-PHI) may have neuroprotective effects on PD through increasing HIF-1α levels. However, the therapeutic benefit of HIF-PHI for PD remains poorly explored due to the lack of proper clinical compounds and understanding of the underlying molecular mechanisms...
2018: Frontiers in Aging Neuroscience
https://www.readbyqxmd.com/read/29755319/ambra1-mediated-mitophagy-counteracts-oxidative-stress-and-apoptosis-induced-by-neurotoxicity-in-human-neuroblastoma-sh-sy5y-cells
#5
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
#6
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/29750731/movement-disorders-in-mitochondrial-disease-a-clinicopathological-correlation
#7
Irene H Flønes, Charalampos Tzoulis
PURPOSE OF REVIEW: The scope of this review is to give an updated account of movement disorders associated with mitochondrial disease, with a particular focus on recently discovered clinicopathological correlations. RECENT FINDINGS: Movement disorders are common clinical manifestations of mitochondrial diseases, in part because of the high vulnerability of neurons controlling motor circuits to mitochondrial respiratory dysfunction and energy failure. Intriguingly, the clinicopathological correlations of movement disorders in mitochondrial disease do not always conform to established neurophysiological knowledge...
May 9, 2018: Current Opinion in Neurology
https://www.readbyqxmd.com/read/29749529/%C3%AE-%C3%A2-synuclein-induces-apoptosis-of-astrocytes-by-causing-dysfunction-of-the-endoplasmic-reticulum%C3%A2-golgi-compartment
#8
Mei Liu, Lixia Qin, Lili Wang, Jieqiong Tan, Hainan Zhang, Jianguang Tang, Xiangmin Shen, Liming Tan, Chunyu Wang
Although previous work has demonstrated that the overexpression of wild‑type or mutant α‑synuclein (α‑syn) can induce cell death via a number of different mechanisms, including oxidative stress, dysfunction of the ubiquitin‑proteasome degradation system, mitochondrial damage and endoplasmic reticulum (ER) stress, research interest has primarily focused on neurons. However, there is accumulating evidence that suggests that astrocytes may be involved in the earliest changes, as well as the progression of Parkinson's disease (PD), though the role of α‑syn in astrocytes has not been widely studied...
May 9, 2018: Molecular Medicine Reports
https://www.readbyqxmd.com/read/29748634/gene-by-environment-interactions-that-disrupt-mitochondrial-homeostasis-cause-neurodegeneration-in-c-elegans-parkinson-s-models
#9
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
#10
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/29735120/movement-disorders-and-neurometabolic-diseases
#11
Celanie K Christensen, Laurence Walsh
Many inherited metabolic diseases or inborn errors of metabolism (IEM) cause movement disorders in children. This review focuses on chorea, dystonia, myoclonus, tremor, and parkinsonism. Broad neurometabolic categories commonly responsible for pediatric movement disorders include mitochondrial cytopathies, organic acidemias, mineral metabolism and transport disorders, neurotransmitter diseases, purine metabolism abnormalities, lipid storage conditions, and creatine metabolism dysfunction. Each movement disorder can be caused by many IEM and several of them can cause multiple movement abnormalities...
April 2018: Seminars in Pediatric Neurology
https://www.readbyqxmd.com/read/29732485/role-of-melatonin-in-aluminum-related-neurodegenerative-disorders-a-review
#12
José L Esparza, Mercedes Gómez, José L Domingo
Aluminum (Al), a potentially neurotoxic element, provokes various adverse effects on human health such as dialysis dementia, osteomalacia, and microcytic anemia. It has been also associated with serious neurodegenerative diseases such as Alzheimer's disease (AD), amyotrophic lateral sclerosis, and Parkinsonism dementia of Guam. The "aluminum hypothesis" of AD assumes that the metal complexes can potentiate the rate of aggregation of amyloid-β (Aβ), enhancing the toxicity of this peptide, and being able of contributing to the pathogenesis of AD...
May 7, 2018: Biological Trace Element Research
https://www.readbyqxmd.com/read/29732085/discovery-of-the-novel-autophagy-inhibitor-aumitin-that-targets-mitochondrial-complex-i
#13
Lucas Robke, Yushi Futamura, Georgios Konstantinidis, Julian Wilke, Harumi Aono, Zhwan Mahmoud, Nobumoto Watanabe, Yao-Wen Wu, Hiroyuki Osada, Luca Laraia, Herbert Waldmann
Macroautophagy is a conserved eukaryotic process for degradation of cellular components in response to lack of nutrients. It is involved in the development of diseases, notably cancer and neurological disorders including Parkinson's disease. Small molecule autophagy modulators have proven to be valuable tools to dissect and interrogate this crucial metabolic pathway and are in high demand. Phenotypic screening for autophagy inhibitors led to the discovery of the novel autophagy inhibitor aumitin. Target identification and confirmation revealed that aumitin inhibits mitochondrial respiration by targeting complex I...
March 21, 2018: Chemical Science
https://www.readbyqxmd.com/read/29731707/the-neuroprotection-of-low-dose-morphine-in-cellular-and-animal-models-of-parkinson-s-disease-through-ameliorating-endoplasmic-reticulum-er-stress-and-activating-autophagy
#14
Bing Wang, Cun-Jin Su, Teng-Teng Liu, Yan Zhou, Yu Feng, Ya Huang, Xu Liu, Zhi-Hong Wang, Li-Hua Chen, Wei-Feng Luo, Tong Liu
Parkinson's disease (PD) is a common neurodegenerative disease characterized the progressive loss of dopaminergic (DA) neurons in the substantia nigra pars compacta (SNc). Brain endogenous morphine biosynthesis was reported to be impaired in PD patients and exogenous morphine attenuated 6-hydroxydopamine (6-OHDA)-induced cell death in vitro . However, the mechanisms underlying neuroprotection of morphine in PD are still unclear. In the present study, we investigated the neuroprotective effects of low-dose morphine in cellular and animal models of PD and the possible underlying mechanisms...
2018: Frontiers in Molecular Neuroscience
https://www.readbyqxmd.com/read/29729423/interaction-between-a-mapt-variant-causing-frontotemporal-dementia-and-mutant-app-affects-axonal-transport
#15
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/29725038/-poly-phenol-digested-metabolites-modulate-alpha-synuclein-toxicity-by-regulating-proteostasis
#16
Diana Macedo, Carolina Jardim, Inês Figueira, A Filipa Almeida, Gordon J McDougall, Derek Stewart, Jose E Yuste, Francisco A Tomás-Barberán, Sandra Tenreiro, Tiago F Outeiro, Cláudia N Santos
Parkinson's disease (PD) is an age-related neurodegenerative disease associated with the misfolding and aggregation of alpha-synuclein (aSyn). The molecular underpinnings of PD are still obscure, but nutrition may play an important role in the prevention, onset, and disease progression. Dietary (poly)phenols revert and prevent age-related cognitive decline and neurodegeneration in model systems. However, only limited attempts were made to evaluate the impact of digestion on the bioactivities of (poly)phenols and determine their mechanisms of action...
May 3, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29719505/cellular-and-molecular-basis-of-neurodegeneration-in-parkinson-disease
#17
REVIEW
Xian-Si Zeng, Wen-Shuo Geng, Jin-Jing Jia, Lei Chen, Peng-Peng Zhang
It has been 200 years since Parkinson disease (PD) was described by Dr. Parkinson in 1817. The disease is the second most common neurodegenerative disease characterized by a progressive loss of dopaminergic neurons in the substantia nigra pars compacta. Although the pathogenesis of PD is still unknown, the research findings from scientists are conducive to understand the pathological mechanisms. It is well accepted that both genetic and environmental factors contribute to the onset of PD. In this review, we summarize the mutations of main seven genes (α-synuclein, LRRK2, PINK1, Parkin, DJ-1, VPS35 and GBA1) linked to PD, discuss the potential mechanisms for the loss of dopaminergic neurons (dopamine metabolism, mitochondrial dysfunction, endoplasmic reticulum stress, impaired autophagy, and deregulation of immunity) in PD, and expect the development direction for treatment of PD...
2018: Frontiers in Aging Neuroscience
https://www.readbyqxmd.com/read/29718367/increased-oxidative-stress-exacerbates-%C3%AE-synuclein-aggregation-in-vivo
#18
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/29714132/mir-7-replacement-therapy-in-parkinson-s-disease
#19
Ricardo Titze-de-Almeida, Simoneide Souza Titze-de-Almeida
The present review examines whether the microRNA 7 (miR-7) holds potential for slowing Parkinson's disease (PD) progression. First, the accurate expression of miR-7 allows for the normal development, physiology, and neurogenesis in the central nervous system, also keeping alpha-synuclein (α-Syn) at the physiological level. Second, patients with PD and parkinsonian MPTP-induced animals exhibit a significant decrease of miR-7 in brain areas associated with dopaminergic neurodegeneration. Depletion of miR-7 in the substantia nigra of clinical samples was related to α-Syn accumulation, loss of dopaminergic cells, and reduction of dopamine in the striatum...
April 30, 2018: Current Gene Therapy
https://www.readbyqxmd.com/read/29710734/evidence-of-neurobiological-changes-in-the-presymptomatic-pink1-knockout-rat
#20
Craig F Ferris, Thomas R Morrison, Sade Iriah, Samantha Malmberg, Praveen Kulkarni, Jochen C Hartner, Malav Trivedi
BACKGROUND: Genetic models of Parkinson's disease (PD) coupled with advanced imaging techniques can elucidate neurobiological disease progression, and can help identify early biomarkers before clinical signs emerge. PTEN-induced putative kinase 1 (PINK1) helps protect neurons from mitochondrial dysfunction, and a mutation in the associated gene is a risk factor for recessive familial PD. The PINK1 knockout (KO) rat is a novel model for familial PD that has not been neuroradiologically characterized for alterations in brain structure/function, alongside behavior, prior to 4 months of age...
April 25, 2018: Journal of Parkinson's Disease
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