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https://www.readbyqxmd.com/read/28627365/mitochondria-metabolic-reprogramming-in-the-formation-of-neurons-from-peripheral-cells-cause-or-consequence-and-the-implications-to-their-utility
#1
REVIEW
Gary E Gibson, Ankita Thakkar
The induction of pluripotent stem cells (iPSC) from differentiated cells such as fibroblasts and their subsequent conversion to neural progenitor cells (NPC) and finally to neurons is intriguing scientifically, and its potential to medicine nearly infinite, but unrealized. A better understanding of the changes at each step of the transformation will enable investigators to use them better to model neurological disease. Each step of conversion from a differentiated cell to an iPSC to a NPC to neurons requires large changes in glycolysis including aerobic glycolysis, the pentose shunt, the tricarboxylic acid cycle, the electron transport chain and in the production of reactive oxygen species (ROS)...
June 13, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28615314/mitochondria-and-reactive-oxygen-species-contribute-to-neurogenic-hypertension
#2
REVIEW
Samuel H H Chan, Julie Y H Chan
Beyond its primary role as fuel generators, mitochondria are engaged in a variety of cellular processes, including redox homeostasis. Mitochondrial dysfunction, therefore, may have a profound impact on high-energy-demanding organs such as the brain. Here, we review the roles of mitochondrial biogenesis and bioenergetics, and their associated signaling in cellular redox homeostasis, and illustrate their contributions to the oxidative stress-related neural mechanism of hypertension, focusing on specific brain areas that are involved in the generation or modulation of sympathetic outflows to the cardiovascular system...
July 2017: Physiology
https://www.readbyqxmd.com/read/28606244/-mitophagy-and-nervous-system-disease
#3
Ming-Xi Li, De-Zhi Mu
Mitophagy is a process during which the cell selectively removes the mitochondria via the mechanism of autophagy. It is crucial to the functional completeness of the whole mitochondrial network and determines cell survival and death. On the one hand, the damaged mitochondria releases pro-apoptotic factors which induce cell apoptosis; on the other hand, the damaged mitochondria eliminates itself via autophagy, which helps to maintain cell viability. Mitophagy is of vital importance for the development and function of the nervous system...
June 2017: Zhongguo Dang Dai Er Ke za Zhi, Chinese Journal of Contemporary Pediatrics
https://www.readbyqxmd.com/read/28600240/neuron-segmentation-with-high-level-biological-priors
#4
Niko Krasowski, Thorsten Beier, Graham Knott, Ullrich Koethe, Fred Hamprecht, Anna Kreshuk
We present a novel approach to the problem of neuron segmentation in image volumes acquired by Electron Microscopy. Existing methods such as agglomerative or correlation clustering rely solely on boundary evidence and have problems where such evidence is lacking (e.g. incomplete staining) or ambiguous (e.g. co-located cell and mitochondria membranes). We investigate if these difficulties can be overcome by means of sparse region appearance cues that differentiate between pre- and postsynaptic neuron segments in mammalian neural tissue...
June 6, 2017: IEEE Transactions on Medical Imaging
https://www.readbyqxmd.com/read/28595361/mitochondrial-dysfunction-underlies-cognitive-defects-as-a-result-of-neural-stem-cell-depletion-and-impaired-neurogenesis
#5
Mireille Khacho, Alysen Clark, Devon S Svoboda, Jason G MacLaurin, Diane C Lagace, David S Park, Ruth S Slack
Mitochondrial dysfunction is a common feature of many genetic disorders that target the brain and cognition. However, the exact role these organelles play in the etiology of such disorders is not understood. Here we show that mitochondrial dysfunction impairs brain development, depletes the adult neural stem cell (NSC) pool and impacts embryonic and adult neurogenesis. Using deletion of the mitochondrial oxidoreductase AIF as a genetic model of mitochondrial and neurodegenerative diseases revealed the importance of mitochondria in multiple steps of the neurogenic process...
June 8, 2017: Human Molecular Genetics
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
#6
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
#7
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
#8
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
#9
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
#10
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
#11
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
#12
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
#13
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
#14
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
#15
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
#16
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
#17
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
#18
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 5mg/kg) for 12 consecutive days, and then on day 13, MPTP (20mg/kg, i...
May 15, 2017: Brain Research
https://www.readbyqxmd.com/read/28315266/sigma-1-receptors-fine-tune-the-neuronal-networks
#19
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
#20
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
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