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https://www.readbyqxmd.com/read/28501723/tangeretin-alters-neuronal-apoptosis-and-ameliorates-the-severity-of-seizures-in-experimental-epilepsy-induced-rats-by-modulating-apoptotic-protein-expressions-regulating-matrix-metalloproteinases-and-activating-the-pi3k-akt-cell-survival-pathway
#1
Xiao-Qian Guo, Yu-Ling Cao, Fang Hao, Zhong-Rui Yan, Mei-Ling Wang, Xue-Wu Liu
PURPOSE: Epilepsy is complex neural disarray categorized by recurring seizures. Despite recent advances in pharmacotherapies for epilepsy, its treatment remains a challenge due to the contrary effects of the drugs. As a result, the identification of novel anti-epileptic drugs (AEDs) with neuroprotective properties and few side effects is of great value. Thus, the present study assessed the treatment effects of tangeretin using a rat model of pilocarpine-induced epilepsy. MATERIALS AND METHODS: Separate groups of male Wistar rats received oral administrations of tangeretin at 50, 100, or 200mg/kg for 10 days and then, on the 10th day, they received an intraperitoneal injection of pilocarpine (30mg/kg)...
May 11, 2017: Advances in Medical Sciences
https://www.readbyqxmd.com/read/28499983/photostimulation-of-mitochondria-as-a-treatment-for-retinal-neurodegeneration
#2
Kathy Beirne, Malgorzata Rozanowska, Marcela Votruba
Absorption of photon energy by neuronal mitochondria leads to numerous downstream neuroprotective effects. Red and near infrared (NIR) light are associated with significantly less safety concerns than light of shorter wavelengths and they are therefore, the optimal choice for irradiating the retina. Potent neuroprotective effects have been demonstrated in various models of retinal damage, by red/NIR light, with limited data from human studies showing its ability to improve visual function. Improved neuronal mitochondrial function, increased blood flow to neural tissue, upregulation of cell survival mediators and restoration of normal microglial function have all been proposed as potential underlying mechanisms of red/NIR light...
May 9, 2017: Mitochondrion
https://www.readbyqxmd.com/read/28495578/expression-pattern-and-functional-analysis-of-fundc1-in-rare-minnow-gobiocypris-rarus
#3
Gongyu Xu, Zhenzhen Li, Jinwen Xiao, Fangqing Li, Weiyuan Ye, Haobin Zhao, Qingchun Zhou, Xueping Zhong
Fundc1 is a mitochondrial outer membrane protein and plays important roles in mitochondria fission and hypoxia-induced mitophagy in mammalian cells. However, there is no relevant report of fundc1 in fish. In the present study, we cloned a 942bp fundc1 cDNA from rare minnow. The cDNA, designated as Grfundc1 cDNA, contains an open reading frame (ORF) of 459bp which encodes a polypeptide of 152 amino acid residues. Comparisons of deduced amino acid sequences demonstrated that Grfundc1 was highly homologous with those of other vertebrates...
May 7, 2017: Gene
https://www.readbyqxmd.com/read/28492551/haploinsufficiency-in-the-mitochondrial-protein-chchd4-reduces-brain-injury-in-a-mouse-model-of-neonatal-hypoxia-ischemia
#4
Yanyan Sun, Tao Li, Cuicui Xie, Yiran Xu, Kai Zhou, Juan Rodriguez, Wei Han, Xiaoyang Wang, Guido Kroemer, Nazanine Modjtahedi, Klas Blomgren, Changlian Zhu
Mitochondria contribute to neonatal hypoxic-ischemic brain injury by releasing potentially toxic proteins into the cytosol. CHCHD4 is a mitochondrial intermembrane space protein that plays a major role in the import of intermembrane proteins and physically interacts with apoptosis-inducing factor (AIF). The purpose of this study was to investigate the impact of CHCHD4 haploinsufficiency on mitochondrial function and brain injury after cerebral hypoxia-ischemia (HI) in neonatal mice. CHCHD4(+/-) and wild-type littermate mouse pups were subjected to unilateral cerebral HI on postnatal day 9...
May 11, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28477283/linking-mitochondrial-dysfunction-to-neurodegeneration-in-lysosomal-storage-diseases
#5
REVIEW
Afshin Saffari, Stefan Kölker, Georg F Hoffmann, Darius Ebrahimi-Fakhari
Lysosomal storage diseases (LSD) are inborn errors of metabolism resulting in multisystem disease. Central nervous system involvement, often with progressive neurodegeneration, accounts for a large portion of the morbidity and mortality seen in many LSD. Available treatments fail to prevent or correct neurologic symptoms and decline. Emerging evidence points to an important role for mitochondrial dysfunction in the pathogenesis and progression of LSD-associated neurodegeneration. Mitochondrial dysfunction in LSD is characterized by alterations in mitochondrial mass, morphology and function...
May 5, 2017: Journal of Inherited Metabolic Disease
https://www.readbyqxmd.com/read/28424571/metabolic-vulnerability-in-the-neurodegenerative-disease-glaucoma
#6
REVIEW
Denise M Inman, Mohammad Harun-Or-Rashid
Axons can be several orders of magnitude longer than neural somas, presenting logistical difficulties in cargo trafficking and structural maintenance. Keeping the axon compartment well supplied with energy also presents a considerable challenge; even seemingly subtle modifications of metabolism can result in functional deficits and degeneration. Axons require a great deal of energy, up to 70% of all energy used by a neuron, just to maintain the resting membrane potential. Axonal energy, in the form of ATP, is generated primarily through oxidative phosphorylation in the mitochondria...
2017: Frontiers in Neuroscience
https://www.readbyqxmd.com/read/28423196/melatonin-enhances-neural-stem-cell-differentiation-and-engraftment-by-increasing-mitochondrial-function
#7
Miguel Mendivil-Perez, Viviana Soto-Mercado, Ana Guerra-Librero, Beatriz I Fernandez-Gil, Javier Florido, Ying-Qiang Shen, Miguel A Tejada, Vivian Capilla-Gonzalez, Iryna Rusanova, José M Garcia-Verdugo, Darío Acuña-Castroviejo, Luis Carlos López, Carlos Velez-Pardo, Marlene Jimenez-Del-Rio, José M Ferrer, Germaine Escames
Neural stem cells (NSCs) are regarded as a promising therapeutic approach to protecting and restoring damaged neurons in neurodegenerative diseases (NDs) such as Parkinson's disease and Alzheimer's disease (PD and AD, respectively). However, new research suggests that NSC differentiation is required to make this strategy effective. Several studies have demonstrated that melatonin increases mature neuronal markers, which reflects NSC differentiation into neurons. Nevertheless, the possible involvement of mitochondria in the effects of melatonin during NSC differentiation has not yet been fully established...
April 19, 2017: Journal of Pineal Research
https://www.readbyqxmd.com/read/28420950/metallothionein-copper-and-alpha-synuclein-in-alpha-synucleinopathies
#8
REVIEW
Yuho Okita, Alexandre N Rcom-H'cheo-Gauthier, Michael Goulding, Roger S Chung, Peter Faller, Dean L Pountney
Metallothioneins (MTs) are proteins that function by metal exchange to regulate the bioavailability of metals, such as zinc and copper. Copper functions in the brain to regulate mitochondria, neurotransmitter production, and cell signaling. Inappropriate copper binding can result in loss of protein function and Cu(I)/(II) redox cycling can generate reactive oxygen species. Copper accumulates in the brain with aging and has been shown to bind alpha-synuclein and initiate its aggregation, the primary aetiological factor in Parkinson's disease (PD), and other alpha-synucleinopathies...
2017: Frontiers in Neuroscience
https://www.readbyqxmd.com/read/28414908/experimental-computational-study-of-carbon-nanotube-effects-on-mitochondrial-respiration-in-silico-nano-qspr-machine-learning-models-based-on-new-raman-spectra-transform-with-markov-shannon-entropy-invariants
#9
Michael González-Durruthy, Luciane C Alberici, Carlos Curti, Zeki Naal, David T Atique-Sawazaki, José M Vázquez-Naya, Humberto González-Díaz, Cristian R Munteanu
The study of selective toxicity of carbon nanotubes (CNTs) on mitochondria (CNT-mitotoxicity) is of major interest for future biomedical applications. In the current work, the mitochondrial oxygen consumption (E3) is measured under three experimental conditions by exposure to pristine and oxidized CNTs (hydroxylated and carboxylated). Respiratory functional assays showed that the information on the CNT Raman spectroscopy could be useful to predict structural parameters of mitotoxicity induced by CNTs. The in vitro functional assays show that the mitochondrial oxidative phosphorylation by ATP-synthase (or state V3 of respiration) was not perturbed in isolated rat-liver mitochondria...
April 25, 2017: Journal of Chemical Information and Modeling
https://www.readbyqxmd.com/read/28414272/regulation-of-mitochondria-dynactin-interaction-and-mitochondrial-retrograde-transport-in-axons
#10
Catherine M Drerup, Amy L Herbert, Kelly R Monk, Alex V Nechiporuk
Mitochondrial transport in axons is critical for neural circuit health and function. While several proteins have been found that modulate bidirectional mitochondrial motility, factors that regulate unidirectional mitochondrial transport have been harder to identify. In a genetic screen, we found a zebrafish strain in which mitochondria fail to attach to the dynein retrograde motor. This strain carries a loss-of-function mutation in actr10, a member of the dynein-associated complex dynactin. The abnormal axon morphology and mitochondrial retrograde transport defects observed in actr10 mutants are distinct from dynein and dynactin mutant axonal phenotypes...
April 17, 2017: ELife
https://www.readbyqxmd.com/read/28366720/brain-energy-metabolism-spurns-fatty-acids-as-fuel-due-to-their-inherent-mitotoxicity-and-potential-capacity-to-unleash-neurodegeneration
#11
REVIEW
Peter Schönfeld, Georg Reiser
The brain uses long-chain fatty acids (LCFAs) to a negligible extent as fuel for the mitochondrial energy generation, in contrast to other tissues that also demand high energy. Besides this generally accepted view, some studies using cultured neural cells or whole brain indicate a moderately active mitochondrial β-oxidation. Here, we corroborate the conclusion that brain mitochondria are unable to oxidize fatty acids. In contrast, the combustion of liver-derived ketone bodies by neural cells is long-known...
March 30, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28336261/methane-rescues-retinal-ganglion-cells-and-limits-retinal-mitochondrial-dysfunction-following-optic-nerve-crush
#12
Ruobing Wang, Qinglei Sun, Fangzhou Xia, Zeli Chen, Jiangchun Wu, Yuelu Zhang, Jiajun Xu, Lin Liu
Secondary degeneration is a common event in traumatic central nervous system disorders, which involves neuronal apoptosis and mitochondrial dysfunction. Exogenous methane exerts the therapeutic effects in many organ injury. Our study aims to investigate the potential neuroprotection of methane in a rat model of optic nerve crush (ONC). Adult male Sprague-Dawley rats were subjected to ONC and administrated intraperitoneally with methane-saturated or normal saline (10 ml/kg) once per day for one week after ONC...
March 20, 2017: Experimental Eye Research
https://www.readbyqxmd.com/read/28322751/neuroprotective-effects-of-2-4-dinitrophenol-in-an-acute-model-of-parkinson-s-disease
#13
Yujeong Lee, Gwangbeom Heo, Kyung Moon Lee, Ah Hyun Kim, Ki Wung Chung, Eunok Im, Hae Young Chung, Jaewon Lee
Neurons depend on mitochondria for homeostasis and survival, and thus, mitochondrial dysfunction has been implicated in neurodegenerative diseases, including Parkinson's disease (PD). Increasing evidence indicates the mitochondrial uncoupler, 2,4-dinitrophenol (DNP), protects neurons against neurodegeneration and enhances neural plasticity. Here, the authors evaluated the protective effects of intraperitoneally (i.p.) administered low dose DNP in an acute mouse model of PD. Mice were administered DNP (1 or 5 mg/kg) for 12 consecutive days, and then on day 13, MPTP (20 mg/kg, i...
March 17, 2017: Brain Research
https://www.readbyqxmd.com/read/28315266/sigma-1-receptors-fine-tune-the-neuronal-networks
#14
Shang-Yi Anne Tsai, Tsung-Ping Su
The endoplasmic reticular (ER) protein sigma-1 receptor (Sig-1R) has been implicated in CNS disorders including but not limited to neurodegenerative diseases, depression , amnesia, and substance abuse. Sig-1Rs are particularly enriched in the specific domain where ER membranes make contacts with the mitochondria (MAM). Within that specific domain, Sig-1Rs play significant roles governing calcium signaling and reactive oxygen species homeostasis to maintain proper neuronal functions. Studies showed that the Sig-1R is pivotal to regulate neuroplasticity and neural survival via multiple aspects of mechanism...
2017: Advances in Experimental Medicine and Biology
https://www.readbyqxmd.com/read/28286181/amplifying-mitochondrial-function-rescues-adult-neurogenesis-in-a-mouse-model-of-alzheimer-s-disease
#15
Kevin Richetin, Manon Moulis, Aurélie Millet, Macarena S Arràzola, Trinovita Andraini, Jennifer Hua, Noélie Davezac, Laurent Roybon, Pascale Belenguer, Marie-Christine Miquel, Claire Rampon
Adult hippocampal neurogenesis is strongly impaired in Alzheimer's disease (AD). In several mouse models of AD, it was shown that adult-born neurons exhibit reduced survival and altered synaptic integration due to a severe lack of dendritic spines. In the present work, using the APPxPS1 mouse model of AD, we reveal that this reduced number of spines is concomitant of a marked deficit in their neuronal mitochondrial content. Remarkably, we show that targeting the overexpression of the pro-neural transcription factor Neurod1 into APPxPS1 adult-born neurons restores not only their dendritic spine density, but also their mitochondrial content and the proportion of spines associated with mitochondria...
June 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28283027/integrated-analysis-of-genetic-behavioral-and-biochemical-data-implicates-neural-stem-cell-induced-changes-in-immunity-neurotransmission-and-mitochondrial-function-in-dementia-with-lewy-body-mice
#16
Anita Lakatos, Natalie R S Goldberg, Mathew Blurton-Jones
We previously demonstrated that transplantation of murine neural stem cells (NSCs) can improve motor and cognitive function in a transgenic model of Dementia with Lewy Bodies (DLB). These benefits occurred without changes in human α-synuclein pathology and were mediated in part by stem cell-induced elevation of brain-derived neurotrophic factor (BDNF). However, instrastriatal NSC transplantation likely alters the brain microenvironment via multiple mechanisms that may synergize to promote cognitive and motor recovery...
March 10, 2017: Acta Neuropathologica Communications
https://www.readbyqxmd.com/read/28250467/automated-synaptic-connectivity-inference-for-volume-electron-microscopy
#17
Sven Dorkenwald, Philipp J Schubert, Marius F Killinger, Gregor Urban, Shawn Mikula, Fabian Svara, Joergen Kornfeld
Teravoxel volume electron microscopy data sets from neural tissue can now be acquired in weeks, but data analysis requires years of manual labor. We developed the SyConn framework, which uses deep convolutional neural networks and random forest classifiers to infer a richly annotated synaptic connectivity matrix from manual neurite skeleton reconstructions by automatically identifying mitochondria, synapses and their types, axons, dendrites, spines, myelin, somata and cell types. We tested our approach on serial block-face electron microscopy data sets from zebrafish, mouse and zebra finch, and computed the synaptic wiring of songbird basal ganglia...
February 27, 2017: Nature Methods
https://www.readbyqxmd.com/read/28224980/alpha-synuclein-prevents-the-formation-of-spherical-mitochondria-and-apoptosis-under-oxidative-stress
#18
Stefanie Menges, Georgia Minakaki, Patrick M Schaefer, Holger Meixner, Iryna Prots, Ursula Schlötzer-Schrehardt, Kristina Friedland, Beate Winner, Tiago F Outeiro, Konstanze F Winklhofer, Christine A F von Arnim, Wei Xiang, Jürgen Winkler, Jochen Klucken
Oxidative stress (OS), mitochondrial dysfunction, and dysregulation of alpha-synuclein (aSyn) homeostasis are key pathogenic factors in Parkinson's disease. Nevertheless, the role of aSyn in mitochondrial physiology remains elusive. Thus, we addressed the impact of aSyn specifically on mitochondrial response to OS in neural cells. We characterize a distinct type of mitochondrial fragmentation, following H2O2 or 6-OHDA-induced OS, defined by spherically-shaped and hyperpolarized mitochondria, termed "mitospheres"...
February 22, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28223472/overexpression-of-sarcoendoplasmic-reticulum-calcium-atpase-2a-promotes-cardiac-sympathetic-neurotransmission-via-abnormal-endoplasmic-reticulum-and-mitochondria-ca-2-regulation
#19
Julia Shanks, Neil Herring, Errin Johnson, Kun Liu, Dan Li, David J Paterson
Reduced cardiomyocyte excitation-contraction coupling and downregulation of the SERCA2a (sarcoendoplasmic reticulum calcium ATPase 2a) is associated with heart failure. This has led to viral transgene upregulation of SERCA2a in cardiomyocytes as a treatment. We hypothesized that SERCA2a gene therapy expressed under a similar promiscuous cytomegalovirus promoter could also affect the cardiac sympathetic neural axis and promote sympathoexcitation. Stellate neurons were isolated from 90 to 120 g male, Sprague-Dawley, Wistar Kyoto, and spontaneously hypertensive rats...
April 2017: Hypertension
https://www.readbyqxmd.com/read/28188219/distinct-effects-of-mir-210-reduction-on-neurogenesis-increased-neuronal-survival-of-inflammation-but-reduced-proliferation-associated-with-mitochondrial-enhancement
#20
Ludmila A Voloboueva, Xiaoyun Sun, Lijun Xu, Yi-Bing Ouyang, Rona G Giffard
Neurogenesis is essential to brain development and plays a central role in the response to brain injury. Stroke and head trauma stimulate proliferation of endogenous neural stem cells (NSCs); however, the survival of young neurons is sharply reduced by postinjury inflammation. Cellular mitochondria are critical to successful neurogenesis and are a major target of inflammatory injury. Mitochondrial protection was shown to improve survival of young neurons. This study tested whether reducing cellular microRNA-210 (miR-210) would enhance mitochondrial function and improve survival of young murine neurons under inflammatory conditions...
March 15, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
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