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https://www.readbyqxmd.com/read/28635542/gene-expression-study-of-mitochondrial-complex-i-in-schizophrenia-and-paranoid-personality-disorder
#1
Arvin Haghighatfard, Sarah Andalib, Mozhdeh Amini Faskhodi, Soha Sadeghi, Amir Hossein Ghaderi, Shadi Moradkhani, Jalal Rostampour, Zeinab Tabrizi, Ali Mahmoodi, Talie Karimi, Zakieh Ghadimi
OBJECTIVES: The aetiology and molecular mechanisms of schizophrenia (SCZ) and paranoid personality disorder (PPD) are not yet clarified. The present study aimed to assess the role of mitochondrial complex I and cell bioenergetic pathways in the aetiology and characteristics of SCZ and PPD. METHODS: mRNA levels of all genomic and mitochondrial genes which encode mitochondrial complex I subunits (44 genes) were assessed in blood in 634 SCZ, 340 PPD patients and 528 non-psychiatric subjects using quantitative real-time PCR, and associated comprehensive psychiatric, neurological and biochemical assessments...
February 20, 2017: World Journal of Biological Psychiatry
https://www.readbyqxmd.com/read/28634226/phostine-pst3-1a-targets-mgat5-and-inhibits-glioblastoma-initiating-cell-invasiveness-and-proliferation
#2
Zahra Hassani, Ali Saleh, Soumaya Turpault, Salim Khiati, Willy Morelle, Jacques Vignon, Jean-Philippe Hugnot, Emmanuelle Uro-Coste, Philippe Legrand, Marcel Delaforge, Séverine Loiseau, Ludovic Clarion, Marc Lecouvey, Jean-Noël Volle, David Virieux, Jean-Luc Pirat, Hugues Duffau, Norbert Bakalara
Glioblastoma multiforme (GBM) is the most common primary malignant brain tumor and accounts for a significant proportion of all primary brain tumors. Median survival after treatment is around 15 months. Remodeling of N-glycans by the N-acetylglucosamine glycosyltransferase (MGAT5) regulates tumoral development. Here, perturbation of MGAT5 enzymatic activity by the small-molecule inhibitor 3-Hydroxy-4,5-bis-benzyloxy-6-benzyloxymethyl-2-phenyl2-oxo-2λ5-[1,2]oxaphosphinane (PST3.1a) restrains GBM growth. In cell based assays it is demonstrated that PST3...
June 20, 2017: Molecular Cancer Research: MCR
https://www.readbyqxmd.com/read/28634116/succinate-induced-neuronal-mitochondrial-fission-and-hexokinase-ii-malfunction-in-ischemic-stroke-therapeutical-effects-of-kaempferol
#3
Bin Wu, Hong Luo, Xu Zhou, Cai-Yi Cheng, Lin Lin, Bao-Lin Liu, Kang Liu, Ping Li, Hua Yang
Mitochondrial dysfunction is known as one of causative factors in ischemic stroke, leading to neuronal cell death. The present work was undertaken to investigate whether succinate induces neuron apoptosis by regulating mitochondrial morphology and function. In neurons, oxygen-glucose deprivation induced succinate accumulation due to the reversal of succinate dehydrogenase (SDH) activation, leading to mitochondrial fission. Kaempferol inhibited mitochondrial fission and maintained mitochondrial HK-II through activation of Akt, and thereby protected neurons from succinate-mediated ischemi injury...
June 17, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28631579/opening-of-katp-channel-regulates-tonic-currents-from-pyramidal-neurons-in-rat-brain
#4
Zhongxia Li, Jiangping Wang, Huimin Yu, Kewen Jiang
BACKGROUND: ATP-sensitive K+ (KATP) channels couple metabolic state to cellular excitability. Activation of neuronal and astrocytic mitochondrial KATP (mitoKATP) channels regulates a variety of neuronal functions. However, less is known about the impact of mitoKATP on tonic γ-aminobutyric acid (GABA) inhibition. Tonic GABA inhibition is mediated by the binding of ambient GABA on extrasynaptic GABA A-type receptors (GABAARs) and is involved in regulating neuronal excitability. METHODS: We determined the impact of activation of KATP channels with diazoxide (DIZ) on tonic inhibition and recorded tonic current from rat cortical layer 5 pyramidal cells by patch-clamp recordings...
June 20, 2017: Canadian Journal of Neurological Sciences. le Journal Canadien des Sciences Neurologiques
https://www.readbyqxmd.com/read/28630030/alzheimer-s-brains-show-inter-related-changes-in-rna-and-lipid-metabolism
#5
Shahar Barbash, Benjamin P Garfinkel, Rotem Maoz, Alon Simchovitz, Bettina Nadorp, Alessandro Guffanti, Estelle R Bennett, Courtney Nadeau, Andreas Türk, Lukas Paul, Torsten Reda, Yan Li, Aron S Buchman, David S Greenberg, Alexander Seitz, David A Bennett, Patrick Giavalisco, Hermona Soreq
Alzheimer's disease (AD) involves changes in both lipid and RNA metabolism, but it remained unknown if these differences associate with AD's cognition and/or post-mortem neuropathology indices. Here, we report RNA-sequencing evidence of inter-related associations between lipid processing, cognition level, and AD neuropathology. In two unrelated cohorts, we identified pathway-enriched facilitation of lipid processing and alternative splicing genes, including the neuronal-enriched NOVA1 and hnRNPA1. Specifically, this association emerged in temporal lobe tissue samples from donors where postmortem evidence demonstrated AD neuropathology, but who presented normal cognition proximate to death...
June 16, 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28628841/mitochondrial-dysfunction-in-autism-spectrum-disorder-clinical-features-and-perspectives
#6
REVIEW
Fiona Hollis, Alexandros K Kanellopoulos, Claudia Bagni
Autism Spectrum Disorder (ASD) is a prototypic pervasive developmental disorder characterized by social interaction, and communication deficits, repetitive, stereotypic patterns of behavior, and impairments in language and development. Clinical studies have identified mitochondrial disturbances at the levels of DNA, activity, complexes, oxidative stress, and metabolites in blood and urine of ASD patients. However, these observations from postmortem brains or peripheral tissues do not provide a direct link between autism and mitochondria...
June 16, 2017: Current Opinion in Neurobiology
https://www.readbyqxmd.com/read/28628137/-antagonistic-effect-of-quercetin-on-pm2-5-toxicity-in-the-rat-s-embryonic-development-in-vitro
#7
A Q Fan, J Q Feng, W Liu, M J Zhang, T Liu, Y L Zhou, Y J Xu
OBJECTIVE: To explore the antagonistic effect of quercetin on fine particulate matter (PM2.5)-induced embryonic developmental toxicity in vitro. METHODS: PM2.5 was collected on glass fiber filters by PM2.5 samplers during the heating period of Dec. 2015 to Mar. 2016 in an area of Haidian District, Beijing City. The sampled filters were cut into 1 cm×3 cm pieces followed by sonication. The PM2.5 suspension was filtered into a 10 cm glass dish through 8 layers of sterile carbasus and stored at -80 °C until freeze drying...
June 18, 2017: Beijing da Xue Xue Bao. Yi Xue Ban, Journal of Peking University. Health Sciences
https://www.readbyqxmd.com/read/28626421/divergent-metabolic-regulation-of-autophagy-and-mtorc1-early-events-in-alzheimer-s-disease
#8
REVIEW
Mai A Shafei, Matthew Harris, Myra E Conway
Alzheimer's disease (AD) is a progressive disease associated with the production and deposition of amyloid β-peptide (Aβ) aggregates and neurofibrillary tangles, which lead to synaptic and neuronal damage. Reduced autophagic flux has been widely associated with the accumulation of autophagic vacuoles (AV), which has been proposed to contribute to aggregate build-up observed in AD. As such, targeting autophagy regulation has received wide review, where an understanding as to how this mechanism can be controlled will be important to neuronal health...
2017: Frontiers in Aging Neuroscience
https://www.readbyqxmd.com/read/28625718/synaptic-functions-of-endocannabinoid-signaling-in-health-and-disease
#9
REVIEW
Alfonso Araque, Pablo E Castillo, Olivier J Manzoni, Raffaella Tonini
Endocannabinoids (eCBs) are a family of lipid molecules that act as key regulators of synaptic transmission and plasticity. They are synthetized "on demand" following physiological and/or pathological stimuli. Once released from postsynaptic neurons, eCBs typically act as retrograde messengers to activate presynaptic type 1 cannabinoid receptors (CB1) and induce short- or long-term depression of neurotransmitter release. Besides this canonical mechanism of action, recent findings have revealed a number of less conventional mechanisms by which eCBs regulate neural activity and synaptic function, suggesting that eCB-mediated plasticity is mechanistically more diverse than anticipated...
June 15, 2017: Neuropharmacology
https://www.readbyqxmd.com/read/28624534/glutaminase-c-overexpression-in-the-brain-induces-learning-deficits-synaptic-dysfunctions-and-neuroinflammation-in-mice
#10
Yi Wang, Yuju Li, Runze Zhao, Beiqing Wu, Blaise Lanoha, Zenghan Tong, Justin Peer, Jianhui Liu, Huangui Xiong, Yunlong Huang, Jialin Zheng
Glutaminolysis, a metabolic process that converts glutamine to glutamate, is particularly important for the central nervous system since glutamate is the major transmitter of excitatory synapses. Glutaminase is the mitochondrial enzyme that catalyzes the first step of glutaminolysis. Two genes encode at least four isoforms of glutaminase in humans. GLS1 gene encodes isoforms kidney-type glutaminase and glutaminase C (GAC) through alternative splicing, whereas GLS2 gene encodes liver-type glutaminase isoforms...
June 14, 2017: Brain, Behavior, and Immunity
https://www.readbyqxmd.com/read/28624490/bioenergetics-dysfunction-mitochondrial-permeability-transition-pore-opening-and-lipid-peroxidation-induced-by-hydrogen-sulfide-as-relevant-pathomechanisms-underlying-the-neurological-dysfunction-characteristic-of-ethylmalonic-encephalopathy
#11
Gabriela Miranda Fernandez Cardoso, Julia Tauana Pletsch, Belisa Parmeggiani, Mateus Grings, Nícolas Manzke Glanzel, Larissa Daniele Bobermin, Alexandre Umpierrez Amaral, Moacir Wajner, Guilhian Leipnitz
Hydrogen sulfide (sulfide) accumulates at high levels in the brains of patients with ethylmalonic encephalopathy (EE). In the present study, we evaluated whether sulfide could disturb energy and redox homeostasis, and induce mitochondrial permeability transition (mPT) pore opening in rat brain aiming to better clarify the neuropathophysiology of EE. Sulfide decreased the activities of citrate synthase and aconitase in rat cerebral cortex mitochondria, and of creatine kinase (CK) in rat cerebral cortex, striatum and hippocampus supernatants...
June 14, 2017: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/28624434/brain-glucose-metabolism-role-of-wnt-signaling-in-the-metabolic-impairment-in-alzheimer-s-disease
#12
REVIEW
Pedro Cisternas, Nibaldo C Inestrosa
The brain is an organ that has a high demand for glucose. In the brain, glucose is predominantly used in energy production, with almost 70% of the energy used by neurons. The importance of the energy requirement in neurons is clearly demonstrated by the fact that all neurodegenerative disorders exhibit a critical metabolic impairment that includes decreased glucose uptake/utilization and decreased mitochondrial activity, with a consequent diminution in ATP production. In fact, in Alzheimer's disease, the measurement of the general metabolic rate of the brain has been reported to be an accurate tool for diagnosis...
June 14, 2017: Neuroscience and Biobehavioral Reviews
https://www.readbyqxmd.com/read/28624412/mild-hypothermia-protects-hippocampal-neurons-against-oxygen-glucose-deprivation-reperfusion-induced-injury-by-improving-lysosomal-function-and-autophagic-flux
#13
Tianen Zhou, Lian Liang, Yanran Liang, Tao Yu, Chaotao Zeng, Longyuan Jiang
Mild hypothermia has been proven to be useful to treat brain ischemia/reperfusion injury. However, the underlying mechanisms have not yet been fully elucidated. The present study was undertaken to determine whether mild hypothermia protects hippocampal neurons against oxygen-glucose deprivation/reperfusion(OGD/R)-induced injury via improving lysosomal function and autophagic flux. The results showed that OGD/R induced the occurrence of autophagy, while the acidic environment inside the lysosomes was altered...
June 15, 2017: Experimental Cell Research
https://www.readbyqxmd.com/read/28623709/the-mechanism-of-neuroprotective-action-of-natural-compounds
#14
REVIEW
Agnieszka Wąsik, Lucyna Antkiewicz-Michaluk
Disturbance of cerebral redox homeostasis is the primary cause of human neurodegenerative disorders, such as Parkinson's disease or Alzheimer's disease. Well known experimental research demonstrates that oxidative stress is a main cause of cell death. A high concentration of reactive oxygen and nitrogen species leads to damage of a lot of proteins, lipids and also DNA. Synthetic compounds used for the treatment in the neurodegenerative diseases failed to meet the hopes they had raised and often exhibit a number of side effects...
April 30, 2017: Pharmacological Reports: PR
https://www.readbyqxmd.com/read/28622174/insufficient-astrocyte-derived-brain-derived-neurotrophic-factor-contributes-to-propofol-induced-neuron-death-through-akt-glycogen-synthase-kinase-3%C3%AE-mitochondrial-fission-pathway
#15
Yanan Liu, Yasheng Yan, Yasuyoshi Inagaki, Sarah Logan, Zeljko J Bosnjak, Xiaowen Bai
BACKGROUND: Growing animal evidence demonstrates that prolonged exposure to propofol during brain development induces widespread neuronal cell death, but there is little information on the role of astrocytes. Astrocytes can release neurotrophic growth factors such as brain-derived neurotrophic factor (BDNF), which can exert the protective effect on neurons in paracrine fashion. We hypothesize that during propofol anesthesia, BDNF released from developing astrocytes may not be sufficient to prevent propofol-induced neurotoxicity...
July 2017: Anesthesia and Analgesia
https://www.readbyqxmd.com/read/28621306/targeted-two-photon-chemical-apoptotic-ablation-of-defined-cell-types-in-vivo
#16
Robert A Hill, Eyiyemisi C Damisah, Fuyi Chen, Alex C Kwan, Jaime Grutzendler
A major bottleneck limiting understanding of mechanisms and consequences of cell death in complex organisms is the inability to induce and visualize this process with spatial and temporal precision in living animals. Here we report a technique termed two-photon chemical apoptotic targeted ablation (2Phatal) that uses focal illumination with a femtosecond-pulsed laser to bleach a nucleic acid-binding dye causing dose-dependent apoptosis of individual cells without collateral damage. Using 2Phatal, we achieve precise ablation of distinct populations of neurons, glia and pericytes in the mouse brain and in zebrafish...
June 16, 2017: Nature Communications
https://www.readbyqxmd.com/read/28620826/individual-amino-acid-supplementation-can-improve-energy-metabolism-and-decrease-ros-production-in-neuronal-cells-overexpressing-alpha-synuclein
#17
Vedad Delic, Jeddidiah W D Griffin, Sandra Zivkovic, Yumeng Zhang, Tam-Anh Phan, Henry Gong, Dale Chaput, Christian Reynes, Vinh B Dinh, Josean Cruz, Eni Cvitkovic, Devon Placides, Ernide Frederic, Hamed Mirzaei, Stanley M Stevens, Umesh Jinwal, Daniel C Lee, Patrick C Bradshaw
Parkinson's disease (PD) is a neurodegenerative disorder characterized by alpha-synuclein accumulation and loss of dopaminergic neurons in the substantia nigra (SN) region of the brain. Increased levels of alpha-synuclein have been shown to result in loss of mitochondrial electron transport chain complex I activity leading to increased reactive oxygen species (ROS) production. WT alpha-synuclein was stably overexpressed in human BE(2)-M17 neuroblastoma cells resulting in increased levels of an alpha-synuclein multimer, but no increase in alpha-synuclein monomer levels...
June 15, 2017: Neuromolecular Medicine
https://www.readbyqxmd.com/read/28620281/inhibition-of-the-mitochondrial-glutamate-carrier-slc25a22-in-astrocytes-leads-to-intracellular-glutamate-accumulation
#18
Emmanuelle Goubert, Yanina Mircheva, Francesco M Lasorsa, Christophe Melon, Emanuela Profilo, Julie Sutera, Hélène Becq, Ferdinando Palmieri, Luigi Palmieri, Laurent Aniksztejn, Florence Molinari
The solute carrier family 25 (SLC25) drives the import of a large diversity of metabolites into mitochondria, a key cellular structure involved in many metabolic functions. Mutations of the mitochondrial glutamate carrier SLC25A22 (also named GC1) have been identified in early epileptic encephalopathy (EEE) and migrating partial seizures in infancy (MPSI) but the pathophysiological mechanism of GC1 deficiency is still unknown, hampered by the absence of an in vivo model. This carrier is mainly expressed in astrocytes and is the principal gate for glutamate entry into mitochondria...
2017: Frontiers in Cellular Neuroscience
https://www.readbyqxmd.com/read/28620275/genome-wide-target-analyses-of-otx2-homeoprotein-in-postnatal-cortex
#19
Akiko Sakai, Ryuichiro Nakato, Yiwei Ling, Xubin Hou, Norikazu Hara, Tomoya Iijima, Yuchio Yanagawa, Ryozo Kuwano, Shujiro Okuda, Katsuhiko Shirahige, Sayaka Sugiyama
Juvenile brain has a unique time window, or critical period, in which neuronal circuits are remodeled by experience. Mounting evidence indicates the importance of neuronal circuit rewiring in various neurodevelopmental disorders of human cognition. We previously showed that Otx2 homeoprotein, essential for brain formation, is recaptured during postnatal maturation of parvalbumin-positive interneurons (PV cells) to activate the critical period in mouse visual cortex. Cortical Otx2 is the only interneuron-enriched transcription factor known to regulate the critical period, but its downstream targets remain unknown...
2017: Frontiers in Neuroscience
https://www.readbyqxmd.com/read/28619113/mechanisms-underlying-extensive-ser129-phosphorylation-in-%C3%AE-synuclein-aggregates
#20
Shigeki Arawaka, Hiroyasu Sato, Asuka Sasaki, Shingo Koyama, Takeo Kato
Parkinson's disease (PD) is characterized neuropathologically by intracellular aggregates of fibrillar α-synuclein, termed Lewy bodies (LBs). Approximately 90% of α-synuclein deposited as LBs is phosphorylated at Ser129 in brains with PD. In contrast, only 4% of total α-synuclein is phosphorylated at Ser129 in brains with normal individuals. It is unclear why extensive phosphorylation occurs in the pathological process of PD. To address this issue, we investigated a mechanism and role of Ser129-phosphorylation in regulating accumulation of α-synuclein...
June 15, 2017: Acta Neuropathologica Communications
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