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https://www.readbyqxmd.com/read/29908245/in-vitro-interaction-and-biocompatibility-of-titanate-nanotubes-with-microglial-cells
#1
S Sruthi, A Loiseau, J Boudon, F Sallem, L Maurizi, P V Mohanan, G Lizard, N Millot
Titanate nanotubes (TiONts) are promising agents for biomedical applications. Microglial activation and associated oxidative burst are major challenges in drug delivery applications across the brain. Here, TiONts were designed for drug delivery systems by functionalizing them with (3-aminopropyl) triethoxysilane (APTES), their interactions and biocompatibility were studied in vitro using murine microglial BV-2 cells. TiONts-APTES exposure resulted in increased ROS production and transient mitochondrial hyperpolarization...
June 13, 2018: Toxicology and Applied Pharmacology
https://www.readbyqxmd.com/read/29908242/medium-chain-triglyceride-diet-reduces-anxiety-like-behaviors-and-enhances-social-competitiveness-in-rats
#2
Fiona Hollis, Ellen Siobhan Mitchell, Carles Canto, Dongmei Wang, Carmen Sandi
Medium-chain triglycerides (MCT) are emerging as unique dietary supplements potentially relevant to improve brain dysfunctions. MCT are converted into ketones and free medium chain fatty acids that, in the brain, are highly effective energy sources to mitochondria and potentially less harmful than glucose metabolism to neurons. Given the recently established link between mitochondrial dysfunction and high anxiety and depression, we set this study to investigate the effectiveness of an MCT-enriched diet to ameliorate anxiety- and depression-related behaviors in rats...
June 13, 2018: Neuropharmacology
https://www.readbyqxmd.com/read/29906515/tspo-expression-and-brain-structure-in-the-psychosis-spectrum
#3
Sina Hafizi, Elisa Guma, Alex Koppel, Tania Da Silva, Michael Kiang, Sylvain Houle, Alan A Wilson, Pablo M Rusjan, M Mallar Chakravarty, Romina Mizrahi
Psychosis is associated with abnormal structural changes in the brain including decreased regional brain volumes and abnormal brain morphology. However, the underlying causes of these structural abnormalities are less understood. The immune system, including microglial activation, has been implicated in the pathophysiology of psychosis. Although previous studies have suggested a connection between peripheral proinflammatory cytokines and structural brain abnormalities in schizophrenia, no in-vivo studies have investigated whether microglial activation is also linked to brain structure alterations previously observed in schizophrenia and its putative prodrome...
June 12, 2018: Brain, Behavior, and Immunity
https://www.readbyqxmd.com/read/29905889/thioredoxin-interacting-protein-mediates-mitochondrion-dependent-apoptosis-in-early-brain-injury-after-subarachnoid-hemorrhage
#4
Yidan Liang, Xudong Che, Qing Zhao, Rami Darwazeh, Hongxia Zhang, Dengzhi Jiang, Jun Zhao, Xiang Xiang, Wang Qin, Liu Liu, Zhaohui He
Early brain injury (EBI) was reported to be the primary cause of high mortality and poor outcomes in subarachnoid hemorrhage (SAH) patients, and apoptosis is regarded as the most important physiopathologic mechanism during EBI. Recently, our team found that thioredoxin-interacting protein (TXNIP) links endoplasmic reticulum stress (ER stress) to neuronal apoptosis and aggravates EBI. However, the other underlying mechanisms remain unknown. Mitochondria are considered to be the central points in integrating apoptotic cell death...
June 15, 2018: Molecular and Cellular Biochemistry
https://www.readbyqxmd.com/read/29905787/induction-of-type-2-iodothyronine-deiodinase-after-status-epilepticus-modifies-hippocampal-gene-expression-in-male-mice
#5
Bruna P P Nascimento, Barbara M L C Bocco, Gustavo W Fernandes, Tatiana L Fonseca, Elizabeth A McAninch, Carolina V Cardoso, Eduardo F Bondan, Renata J Nassif, Roberta M Cysneiros, Antonio C Bianco, Miriam O Ribeiro
Status Epilepticus (SE) is an abnormally prolonged seizure that results from either a failure of mechanisms that terminate seizures or from initiating mechanisms that inherently lead to prolonged seizures. Here we report that mice experiencing a 3 h SE caused by pilocarpine exhibit a rapid increase in expression of type 2 iodothyronine deiodinase gene (Dio2) and a decrease in the expression of type 3 iodothyronine deiodinase gene (Dio3) in hippocampus, amygdala and prefrontal cortex. Type 3 iodothyronine deiodinase (D3) in hippocampal sections was seen concentrated in the neuronal nuclei, typical of ischemic injury of the brain...
June 13, 2018: Endocrinology
https://www.readbyqxmd.com/read/29904371/hypothalamic-mitochondrial-dysfunction-as-a-target-in-obesity-and-metabolic-disease
#6
REVIEW
Juan Cunarro, Sabela Casado, Javier Lugilde, Sulay Tovar
Mitochondria are important organelles for the adaptation to energy demand that play a central role in bioenergetics metabolism. The mitochondrial architecture and mitochondrial machinery exhibits a high degree of adaptation in relation to nutrient availability. On the other hand, its disruption markedly affects energy homeostasis. The brain, more specifically the hypothalamus, is the main hub that controls energy homeostasis. Nevertheless, until now, almost all studies in relation to mitochondrial dysfunction and energy metabolism have focused in peripheral tissues like brown adipose tissue, muscle, and pancreas...
2018: Frontiers in Endocrinology
https://www.readbyqxmd.com/read/29904091/naloxone-attenuates-ischemic-brain-injury-in-rats-through-suppressing-the-nik-ikk%C3%AE-nf-%C3%AE%C2%BAb-and-neuronal-apoptotic-pathways
#7
Xuan Wang, Zu-Jun Sun, Jun-Lu Wu, Wen-Qiang Quan, Wei-Dong Xiao, Helen Chew, Cui-Min Jiang, Dong Li
Although naloxone has been documented to exert neuroprotection in animal model of cerebral ischemia, the mechanism is not well understood. In this present study we investigated whether naloxone affected the mitochondrial apoptotic pathway in ischemic brain injury of rats. SD rats were subjected to a permanent middle cerebral artery occlusion surgery, and received naloxone (0.5, 1, 2 mg/kg, i.v.) immediately after ischemia. Neurological deficits were evaluated 24 h after ischemia using the McGraw Stroke Index, and then the rats were killed, and the brains were collected for further analyses...
June 14, 2018: Acta Pharmacologica Sinica
https://www.readbyqxmd.com/read/29903725/human-primitive-brain-displays-negative-mitochondrial-nuclear-expression-correlation-of-respiratory-genes
#8
Gilad Barshad, Amit Blumberg, Tal Cohen, Dan Mishmar
Oxidative phosphorylation (OXPHOS), a fundamental energy source in all human tissues, requires interactions between mitochondrial (mtDNA) and nuclear (nDNA)-encoded protein subunits. Although such interactions are fundamental to OXPHOS, bi-genomic co-regulation is poorly understood. To address this question, we analyzed ~8,500 RNA-seq experiments from 48 human body sites. Despite well-known variation in mitochondrial activity, quantity and morphology, we found overall positive mtDNA-nDNA OXPHOS genes' co-expression across human tissues...
June 14, 2018: Genome Research
https://www.readbyqxmd.com/read/29902488/tgf-%C3%AE-and-bmp-signals-regulate-insect-diapause-through-smad1-pou-tfam-pathway
#9
Hai-Yin Li, Xian-Wu Lin, Shao-Lei Geng, Wei-Hua Xu
The transforming growth factor-β (TGF-β) superfamily signaling pathway contains two general branches, known as TGF-β and bone morphogenetic protein (BMP), that regulate development in animals. It is well known that TGF-β superfamily signaling participates in the regulation of dauer (lifespan extension) in Caenorhabditis elegans, but little is known about the molecular mechanisms of lifespan extension in the pathway. Diapause, a programmed developmental arrest in insects, is similar to dauer in C. elegans...
June 11, 2018: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/29902125/silencing-of-lncrna-bdnf-as-attenuates-a%C3%AE-25-35-induced-neurotoxicity-in-pc12-cells-by-suppressing-cell-apoptosis-and-oxidative-stress
#10
Cong-Cong Guo, Chun-Hong Jiao, Zhen-Mei Gao
OBJECTIVE: To explore the effects of long non-coding RNA (lncRNA) brain-derived neurotrophic factor anti-sense (BDNF-AS) on the Aβ25-35 -induced neurotoxicity in PC12 cells. METHODS: PC12 cells were induced by Aβ25-35 to construct cell injury models of Alzheimer's disease (AD), and then transfected with siRNA-BDNF-AS. Quantitative real-time polymerase chain reaction (qRT-PCR) was employed to detect the expressions of BDNF-AS and BDNF. Besides, 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and Hoechst33342 staining were utilized to analyze the cell viability and apoptosis, respectively, Western blotting to evaluate the protein expressions, immunofluorescence to assess the Cytochrome C (Cyt C) release, and Rhodamine 123 (Rh123) to measure the mitochondrial membrane potential (MMP)...
June 14, 2018: Neurological Research
https://www.readbyqxmd.com/read/29896715/measurement-of-mitochondrial-toxicity-parameters-in-embryonic-hippocampus
#11
Ahmad Salimi, Jalal Pourahmad
Recent discoveries have focused on mitochondria functions in the neuroscience research for approaches to study mitochondria dysfunction in neurodegenerative diseases. Mitochondrion is one of the organelles that is possibly worst affected in cognitive impairments. These are known as "powerhouse" of the cell as they are the main source of generation of ATP through aerobic respiration. They have role in oxidative phosphorylation and metabolism, they play central role in cell differentiation, apoptosis, oxygen sensing and detoxification of reactive oxygen species, innate immunity, mitochondrial matrix calcium, and maintenance of cell quality and regulation of cytoplasmic...
2018: Methods in Molecular Biology
https://www.readbyqxmd.com/read/29896232/relationship-between-changes-in-mitochondrial-function-and-hippocampal-neuronal-apoptosis-after-recurrent-convulsion-during-developmental-stage
#12
Yueying Liu, Jieru Chen, Meifang Jin, Zhenhong Li, Tian Tian, Lili Li, Hong Ni
The aim of the present study was to establish a recurrent convulsion model during the developmental stage using inhalation of flurothyl, and to observe the relationship between the changes in mitochondrial function in hippocampal neurons and hippocampal neuronal apoptosis after recurrent convulsion. A total of 36 Sprague-Dawley male rats were selected and randomly divided into the control (NS) group and recurrent-seizure (RS) group for 0, 1.5, 3, 12 and 24 h. After the last seizure the rats were subdivided with 6 animals in each group...
July 2018: Experimental and Therapeutic Medicine
https://www.readbyqxmd.com/read/29895494/neuroprotective-effect-of-a-standardized-extract-of-centella-asiatica-eca233-in-rotenone-induced-parkinsonism-rats
#13
Narudol Teerapattarakan, Hattaya Benya-Aphikul, Rossarin Tansawat, Oraphan Wanakhachornkrai, Mayuree H Tantisira, Ratchanee Rodsiri
BACKGROUND: Mitochondrial dysfunction and reactive oxygen species (ROS) generation cause dopaminergic neurodegeneration in Parkinson's disease. The neuroprotective approach is a promising strategy to slow disease progression in Parkinson's disease. A standardized extract of Centella asiatica ECa233 has been previously reported to have pharmacological effects in the central nervous system. PURPOSE: This study aimed to determine the neuroprotective effect and mechanisms of ECa233 in rotenone-induced parkinsonism rats...
May 15, 2018: Phytomedicine: International Journal of Phytotherapy and Phytopharmacology
https://www.readbyqxmd.com/read/29895248/tau-positive-neurons-show-marked-mitochondrial-loss-and-nuclear-degradation-in-alzheimer-s-disease
#14
Melissa Wee, Fariba Chegini, John H T Power, Shohreh Majd
BACKGROUND: Alzheimer's disease (AD) pathology consists of intraneuronal neurofibrillary tangles, made of hyperphosphorylated tau and extracellular accumulation of beta amyloid (Aβ) in Aβ plaques. There is an extensive debate as to which pathology initiates and responsible for cellular loss in AD. METHODS: Using confocal and light microscopy, post mortem brains from control and AD cases, an antibody to SOD2 as a marker for mitochondria and an antibody to all forms of tau, we analyzed mitochondrial density in tau positive neurons along with nuclear degradation by calculating the raw integrative density...
June 12, 2018: Current Alzheimer Research
https://www.readbyqxmd.com/read/29892158/modification-of-%C3%AE-synuclein-by-lipid-peroxidation-products-derived-from-polyunsaturated-fatty-acids-promotes-toxic-oligomerization-its-relevance-to-parkinson-disease
#15
REVIEW
Masayo Shamoto-Nagai, Shinsuke Hisaka, Makoto Naoi, Wakako Maruyama
Recently, toxic α-synuclein oligomer, which can mediate cell-to-cell propagation is suggested to cause sporadic Parkinson disease. α-Synuclein interacts with membrane lipids especially polyunsaturated fatty acids to stabilize its three-dementional structure. Peroxidation of polyunsaturated fatty acids may reduce their affinity to α-synuclein and peroxidation byproducts might modify α-synuclein. 4-Hydroxy-2-nonenal derived from n -6 polyunsaturated fatty acids was reported to modify α-synuclein to produce a toxic oligomer...
May 2018: Journal of Clinical Biochemistry and Nutrition
https://www.readbyqxmd.com/read/29892070/an-inhibitor-of-oxidative-phosphorylation-exploits-cancer-vulnerability
#16
Jennifer R Molina, Yuting Sun, Marina Protopopova, Sonal Gera, Madhavi Bandi, Christopher Bristow, Timothy McAfoos, Pietro Morlacchi, Jeffrey Ackroyd, Ahmed-Noor A Agip, Gheath Al-Atrash, John Asara, Jennifer Bardenhagen, Caroline C Carrillo, Christopher Carroll, Edward Chang, Stefan Ciurea, Jason B Cross, Barbara Czako, Angela Deem, Naval Daver, John Frederick de Groot, Jian-Wen Dong, Ningping Feng, Guang Gao, Jason Gay, Mary Geck Do, Jennifer Greer, Virginia Giuliani, Jing Han, Lina Han, Verlene K Henry, Judy Hirst, Sha Huang, Yongying Jiang, Zhijun Kang, Tin Khor, Sergej Konoplev, Yu-Hsi Lin, Gang Liu, Alessia Lodi, Timothy Lofton, Helen Ma, Mikhila Mahendra, Polina Matre, Robert Mullinax, Michael Peoples, Alessia Petrocchi, Jaime Rodriguez-Canale, Riccardo Serreli, Thomas Shi, Melinda Smith, Yoko Tabe, Jay Theroff, Stefano Tiziani, Quanyun Xu, Qi Zhang, Florian Muller, Ronald A DePinho, Carlo Toniatti, Giulio F Draetta, Timothy P Heffernan, Marina Konopleva, Philip Jones, M Emilia Di Francesco, Joseph R Marszalek
Metabolic reprograming is an emerging hallmark of tumor biology and an actively pursued opportunity in discovery of oncology drugs. Extensive efforts have focused on therapeutic targeting of glycolysis, whereas drugging mitochondrial oxidative phosphorylation (OXPHOS) has remained largely unexplored, partly owing to an incomplete understanding of tumor contexts in which OXPHOS is essential. Here, we report the discovery of IACS-010759, a clinical-grade small-molecule inhibitor of complex I of the mitochondrial electron transport chain...
June 11, 2018: Nature Medicine
https://www.readbyqxmd.com/read/29892051/ant1-mutant-mice-bridge-the-mitochondrial-and-serotonergic-dysfunctions-in-bipolar-disorder
#17
Tomoaki M Kato, Mie Kubota-Sakashita, Noriko Fujimori-Tonou, Fumihito Saitow, Satoshi Fuke, Akira Masuda, Shigeyoshi Itohara, Hidenori Suzuki, Tadafumi Kato
Although mitochondrial and serotonergic dysfunctions have been implicated in the etiology of bipolar disorder (BD), the relationship between these unrelated pathways has not been elucidated. A family of BD and chronic progressive external ophthalmoplegia (CPEO) caused by a mutation of the mitochondrial adenine nucleotide translocator 1 (ANT1, SLC25A4) implicated that ANT1 mutations confer a risk of BD. Here, we sequenced ANT1 in 324 probands of NIMH bipolar disorder pedigrees and identified two BD patients carrying heterozygous loss-of-function mutations...
June 11, 2018: Molecular Psychiatry
https://www.readbyqxmd.com/read/29891925/cadmium-induced-apoptosis-in-neuronal-cells-is-mediated-by-fas-fasl-mediated-mitochondrial-apoptotic-signaling-pathway
#18
Yan Yuan, Yajing Zhang, Shiwen Zhao, Jie Chen, Jinlong Yang, Tao Wang, Hui Zou, Yi Wang, Jianhong Gu, Xuezhong Liu, Jianchun Bian, Zongping Liu
Cadmium (Cd) is a toxic metal capable of damaging brain. Studies have demonstrated that Cd can induce apoptosis in neuronal cells. The CD95/APO-1 (Fas)/Fas Ligand (FasL) signaling pathway is one of the primary apoptosis pathways, but the role and regulatory mechanism of this pathway in neuronal cells remain unclear. Here, we demonstrated the underlying mechanism of the Fas/FasL system involving the mitochondrial apoptotic pathway in neuronal cells. Primary rat cerebral cortical neurons and PC12 cells were exposed to Cd, which significantly activated expression of Fas, FasL, Fas-associated death domain (FADD) and cleaved caspase-8...
June 11, 2018: Scientific Reports
https://www.readbyqxmd.com/read/29890214/evolutionary-perspective-on-sex-differences-in-the-expression-of-neurological-diseases
#19
REVIEW
David C Geary
Sex-specific brain and cognitive deficits emerge with malnutrition, some infectious and neurodegenerative diseases, and often with prenatal or postnatal toxin exposure. These deficits are described in disparate literatures and are generally not linked to one another. Sexual selection may provide a unifying framework that integrates our understanding of these deficits and provides direction for future studies of sex-specific vulnerabilities. Sexually selected traits are those that have evolved to facilitate competition for reproductive resources or that influence mate choices, and are often larger and more complex than other traits...
June 8, 2018: Progress in Neurobiology
https://www.readbyqxmd.com/read/29886547/identification-and-characterization-of-amyloid-%C3%AE-accumulation-in-synaptic-mitochondria
#20
Shi Fang Yan, Firoz Akhter, Alexander A Sosunov, Shirley ShiDu Yan
Mitochondrial and synaptic dysfunction is an early pathological feature of Alzheimer's disease (AD). Accumulation of amyloid beta-peptide (Aβ) in mitochondria, particularly in synaptic mitochondria, potentiates and amplifies synaptic injury and disruption of synaptic transmission, leading to synaptic dysfunction and ultimately to synaptic failure. Thus, determination of the presence and levels of Aβ in synaptic mitochondria associated with amyloid pathology is important for studying mitochondrial amyloid pathology...
2018: Methods in Molecular Biology
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