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https://www.readbyqxmd.com/read/28433663/mitochondrial-mechanisms-of-neuronal-rescue-by-f-68-a-hydrophilic-pluronic-block-co-polymer-following-acute-substrate-deprivation
#1
REVIEW
Janice C Wang, Vytautas P Bindokas, Matthew Skinner, Todd Emrick, Jeremy D Marks
Global brain ischemia can lead to widespread neuronal death and poor neurologic outcomes in patients. Despite detailed understanding of the cellular and molecular mechanisms mediating neuronal death following focal and global brain hypoxia-ischemia, treatments to reduce ischemia-induced brain injury remain elusive. One pathway central to neuronal death following global brain ischemia is mitochondrial dysfunction, one consequence of which is the cascade of intracellular events leading to mitochondrial outer membrane permeabilization...
April 19, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28432138/inhibition-of-drp1-ameliorates-synaptic-depression-a%C3%AE-deposition-and-cognitive-impairment-in-alzheimer-s-disease-model
#2
Seung-Hyun Baek, So Jung Park, Jae In Jeong, Sung Hyun Kim, Jihoon Han, Jae Won Kyung, Sang-Ha Baik, Yuri Choi, Bo-Youn Choi, Jinsu Park, Gahee Bahn, Ji Hyun Shin, Doo Sin Jo, Joo-Yong Lee, Choon-Gon Jang, Thiruma V Arumugam, Jongpil Kim, Jeung-Whan Han, Jae-Young Koh, Dong-Hyung Cho, Dong-Gyu Jo
Excessive mitochondrial fission is a prominent early event, and contributes to mitochondrial dysfunction, synaptic failure and neuronal cell death in the progression of Alzheimer's disease (AD). However, it remains to be determined whether inhibition of excessive mitochondrial fission is beneficial in mammal models of AD. To determine whether dynamin-related protein 1 (Drp1), a key regulator of mitochondrial fragmentation, can be a disease-modifying therapeutic target for AD, we examine the effects of Drp1 inhibitor on mitochondrial and synaptic dysfunctions induced by oligomeric β-amyloid (Aβ) in neurons, and neuropathology and cognitive functions in APP/PS1 double transgenic AD mice...
April 21, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/28431972/mitochondrial-energy-metabolism-of-rat-hippocampus-after-treatment-with-the-antidepressants-desipramine-and-fluoxetine
#3
Roberto Federico Villa, Federica Ferrari, Laura Bagini, Antonella Gorini, Nicoletta Brunello, Fabio Tascedda
Alterations in mitochondrial functions have been hypothesized to participate in the pathogenesis of depression, because brain bioenergetic abnormalities have been detected in depressed patients by neuroimaging in vivo studies. However, this hypothesis is not clearly demonstrated in experimental studies: some suggest that antidepressants are inhibitors of mitochondrial metabolism, while others observe the opposite. In this study, the effects of 21-day treatment with desipramine (15 mg/kg) and fluoxetine (10 mg/kg) were examined on the energy metabolism of rat hippocampus, evaluating the catalytic activity of regulatory enzymes of mitochondrial energy-yielding metabolic pathways...
April 18, 2017: Neuropharmacology
https://www.readbyqxmd.com/read/28427981/ultrastructure-of-pericystic-or-intracystic-blood-vessels-in-epidermoid-cysts-a-transmission-electron-microscopy-study-laboratory-investigation
#4
Xiao-Hui Ren, Jun Ma, Chun Zeng, Yi-Lin Sun, Song Lin
OBJECTIVES: Recently, we reported the tendency towards the spontaneous hemorrhage in both pre- and post-operative periods of patients with intracranial epidermoid cyst (EC). According to our experience this tendency of spontaneous hemorrhage was partly due to the pathologic blood vessels adjacent to the EC. This article was designed to testify this hypothesis. MATERIALS & METHODS: 23 removable pericystic or intracystic blood vessels from 17 EC patients were collected during surgery, and then were examined by transmission electron microscope...
April 17, 2017: World Neurosurgery
https://www.readbyqxmd.com/read/28424571/metabolic-vulnerability-in-the-neurodegenerative-disease-glaucoma
#5
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/28423937/concordance-of-several-subcellular-interactions-initiates-alzheimer-s-dementia-their-reversal-requires-combination-treatment
#6
W J Fessel
The pathogenesis of Alzheimer's disease involves multiple pathways that, at the macrolevel, include decreased proliferation plus increased loss affecting neurons, astrocytes, and capillaries and, at the subcellular level, involve several elements: amyloid/amyloid precursor protein, presenilins, the unfolded protein response, the ubiquitin/proteasome system, the Wnt/catenin system, the Notch signaling system, mitochondria, mitophagy, calcium, and tau. Data presented show the intimate, anatomical interactions between neurons, astrocytes, and capillaries; the interactions between the several subcellular factors affecting those cells; and the treatments that are currently available and that might correct dysfunctions in the subcellular factors...
May 2017: American Journal of Alzheimer's Disease and Other Dementias
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/28412312/updates-to-a-13-c-metabolic-flux-analysis-model-for-evaluating-energy-metabolism-in-cultured-cerebellar-granule-neurons-from-neonatal-rats
#9
Mika B Jekabsons, Hoda M Gebril, Yan-Hong Wang, Bharathi Avula, Ikhlas A Khan
A hexose phosphate recycling model previously developed to infer fluxes through the major glucose consuming pathways in cultured cerebellar granule neurons (CGNs) from neonatal rats metabolizing [1,2-(13)C2]glucose was revised by considering reverse flux through the non-oxidative pentose phosphate pathway (PPP) and symmetrical succinate oxidation within the tricarboxylic acid (TCA) cycle. The model adjusts three flux ratios to effect (13)C distribution in the hexose, pentose, and triose phosphate pools, and in TCA cycle malate to minimize the error between predicted and measured (13)C labeling in exported lactate (i...
April 12, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28409745/mitochondria-division-inhibitor-1-protects-against-amyloid-%C3%AE-induced-mitochondrial-fragmentation-and-synaptic-damage-in-alzheimer-s-disease
#10
P Hemachandra Reddy, Maria Manczak, XiangLing Yin
The purpose our study was to determine the protective effects of mitochondria division inhibitor 1 (Mdivi1) in Alzheimer's disease (AD). Mdivi1 is hypothesized to reduce excessive fragmentation of mitochondria and mitochondrial dysfunction in AD neurons. Very little is known about whether Mdivi1 can confer protective effects in AD. In the present study, we sought to determine the protective effects of Mdivi1 against amyloid-β (Aβ)- and mitochondrial fission protein, dynamin-related protein 1 (Drp1)-induced excessive fragmentation of mitochondria in AD progression...
April 10, 2017: Journal of Alzheimer's Disease: JAD
https://www.readbyqxmd.com/read/28409447/isolation-of-peroxisomes-from-mouse-brain-using-a-continuous-nycodenz-gradient-a-comparison-to-the-isolation-of-liver-and-kidney-peroxisomes
#11
Miriam J Schönenberger, Werner J Kovacs
In the central nervous system (CNS) peroxisomes are present in all cell types, namely neurons, oligodendrocytes, astrocytes, microglia, and endothelial cells. Brain peroxisomes are smaller in size compared to peroxisomes from other tissues and are therefore referred to as microperoxisomes. We have established a purification procedure to isolate highly purified peroxisomes from the central nervous system that are well separated from the endoplasmic reticulum and mitochondria and are free of myelin contamination...
2017: Methods in Molecular Biology
https://www.readbyqxmd.com/read/28408307/mitochondrial-respiratory-chain-disorganization-in-parkinson-s-disease-relevant-pink1-and-dj1-mutants
#12
Irene Lopez-Fabuel, Lucia Martin-Martin, Monica Resch-Beusher, Garikoitz Azkona, Rosario Sanchez-Pernaute, Juan P Bolaños
Brain mitochondrial complex I (CI) damage is associated with the loss of the dopaminergic neurons of the Substantia Nigra in Parkinson's Disease (PD) patients. However, whether CI inhibition is associated with any alteration of the mitochondrial respiratory chain (MRC) organization in PD patients is unknown. To address this issue, here we analyzed the MRC by blue native gel electrophoresis (BNGE) followed by western blotting, in mitochondria purified from fibroblasts of patients harboring PD-relevant Pink1 mutations...
April 10, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28401402/ischemia-reperfusion-induced-translocation-of-pkc%C3%AE-ii-to-mitochondria-as-an-important-mediator-of-a-protective-signaling-mechanism-in-an-ischemia-resistant-region-of-the-hippocampus
#13
Olga Krupska, Anna Sarnowska, Bartlomiej Fedorczyk, Magdalena Gewartowska, Aleksandra Misicka, Barbara Zablocka, Malgorzata Beresewicz
Emerging reports indicate that activated PKC isoforms that translocate to the mitochondria are pro- or anti-apoptotic to mitochondrial function. Here, we concentrate on the role of PKCβ translocated to mitochondria in relation to the fate of neurons following cerebral ischemia. As we have demonstrated previously ischemia/reperfusion injury (I/R) results in translocation of PKCβ from cytoplasm to mitochondria, but only in ischemia-resistant regions of the hippocampus (CA2-4, DG), we hypothesize that this translocation may be a mediator of a protective signaling mechanism in this region...
April 12, 2017: Neurochemical Research
https://www.readbyqxmd.com/read/28399880/quantitative-proteomic-analysis-of-parkin-substrates-in-drosophila-neurons
#14
Aitor Martinez, Benoit Lectez, Juanma Ramirez, Oliver Popp, James D Sutherland, Sylvie Urbé, Gunnar Dittmar, Michael J Clague, Ugo Mayor
BACKGROUND: Parkin (PARK2) is an E3 ubiquitin ligase that is commonly mutated in Familial Parkinson's Disease (PD). In cell culture models, Parkin is recruited to acutely depolarised mitochondria by PINK1. PINK1 activates Parkin activity leading to ubiquitination of multiple proteins, which in turn promotes clearance of mitochondria by mitophagy. Many substrates have been identified using cell culture models in combination with depolarising drugs or proteasome inhibitors, but not in more physiological settings...
April 11, 2017: Molecular Neurodegeneration
https://www.readbyqxmd.com/read/28396174/sirt3-confers-protection-against-neuronal-ischemia-by-inducing-autophagy-involvement-of-the-ampk-mtor-pathway
#15
Shu-Hui Dai, Tao Chen, Xia Li, Kang-Yi Yue, Peng Luo, Li-Kun Yang, Jie Zhu, Yu-Hai Wang, Zhou Fei, Xiao-Fan Jiang
Sirtuin3 (Sirt3) is a member of the silent information regulator 2 (Sir2) family of proteins located in mitochondria that influences almost every major aspect of mitochondrial biology, including ATP generation and reactive oxygen species (ROS) production. Our previous study showed that Sirt3 exerts protective effects against oxidative stress in neuronal cells. In this study, we investigated the role of Sirt3 in neuronal ischemia using an oxygen and glucose deprivation (OGD) model. Sirt3 was up-regulated by OGD and overexpression of Sirt3 through lentivirus transfection significantly reduced OGD-induced lactate dehydrogenase (LDH) release and neuronal apoptosis...
April 7, 2017: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/28395670/absence-of-physiological-ca-2-transients-is-an-initial-trigger-for-mitochondrial-dysfunction-in-skeletal-muscle-following-denervation
#16
Chehade Karam, Jianxun Yi, Yajuan Xiao, Kamal Dhakal, Lin Zhang, Xuejun Li, Carlo Manno, Jiejia Xu, Kaitao Li, Heping Cheng, Jianjie Ma, Jingsong Zhou
BACKGROUND: Motor neurons control muscle contraction by initiating action potentials in muscle. Denervation of muscle from motor neurons leads to muscle atrophy, which is linked to mitochondrial dysfunction. It is known that denervation promotes mitochondrial reactive oxygen species (ROS) production in muscle, whereas the initial cause of mitochondrial ROS production in denervated muscle remains elusive. Since denervation isolates muscle from motor neurons and deprives it from any electric stimulation, no action potentials are initiated, and therefore, no physiological Ca(2+) transients are generated inside denervated muscle fibers...
April 10, 2017: Skeletal Muscle
https://www.readbyqxmd.com/read/28393656/punicalagin-reduces-h2o2-induced-cytotoxicity-and-apoptosis-in-pc12-cells-by-modulating-the-levels-of-reactive-oxygen-species
#17
Maria Elisabetta Clementi, Giovambattista Pani, Beatrice Sampaolese, Giuseppe Tringali
BACKGROUND: Oxidative stress has long been linked to neuronal cell death in many neurodegenerative diseases. Antioxidant conventional supplements are poorly effective in preventing neuronal damage caused by oxidative stress due to their inability to cross the blood brain barrier. Hence the use of molecules extracted from plants and fruits such as phenolics, flavonoids, and terpenoids compounds constitute a new wave of antioxidant therapies to defend against free radicals. OBJECTIVE: In this study we examined the effects of punicalagin, a ellagitannin isolated from the pomegranate juice, on a rat adrenal pheochromocytoma cell line, treated with hydrogen peroxide, evaluating the viability, oxidation potential, mitochondrial function, and eventual apoptosis...
April 9, 2017: Nutritional Neuroscience
https://www.readbyqxmd.com/read/28387723/classical-and-novel-tspo-ligands-for-the-mitochondrial-tspo-can-modulate-nuclear-gene-expression-implications-for-mitochondrial-retrograde-signaling
#18
Nasra Yasin, Leo Veenman, Sukhdev Singh, Maya Azrad, Julia Bode, Alex Vainshtein, Beatriz Caballero, Ilan Marek, Moshe Gavish
It is known that knockdown of the mitochondrial 18 kDa translocator protein (TSPO) as well as TSPO ligands modulate various functions, including functions related to cancer. To study the ability of TSPO to regulate gene expression regarding such functions, we applied microarray analysis of gene expression to U118MG glioblastoma cells. Within 15 min, the classical TSPO ligand PK 11195 induced changes in expression of immediate early genes and transcription factors. These changes also included gene products that are part of the canonical pathway serving to modulate general gene expression...
April 7, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28386319/tetrahydrocurcumin-reduces-oxidative-stress-induced-apoptosis-via-the-mitochondrial-apoptotic-pathway-by-modulating-autophagy-in-rats-after-traumatic-brain-injury
#19
Yongyue Gao, Zong Zhuang, Shanting Gao, Xiang Li, Zihuan Zhang, Zhennan Ye, Liwen Li, Chao Tang, Mengliang Zhou, Xiao Han, Jie Li
Tetrahydrocurcumin (THC) has been identified as a multi-functional neuroprotective agent in numerous neurological disorders. Oxidative stress as a result of injury may induce neuronal apoptosis after traumatic brain injury (TBI). Treatment with THC may improve neurological function following TBI by attenuating oxidative stress and apoptosis and by enhancing autophagy. The purpose of this study was to investigate the mechanism of neuroprotection by THC against oxidative stress-induced neuronal apoptosis after TBI...
2017: American Journal of Translational Research
https://www.readbyqxmd.com/read/28384611/bid-links-ferroptosis-to-mitochondrial-cell-death-pathways
#20
Sandra Neitemeier, Anja Jelinek, Vincenzo Laino, Lena Hoffmann, Ina Eisenbach, Roman Eying, Goutham K Ganjam, Amalia M Dolga, Sina Oppermann, Carsten Culmsee
Ferroptosis has been defined as an oxidative and iron-dependent pathway of regulated cell death that is distinct from caspase-dependent apoptosis and established pathways of death receptor-mediated regulated necrosis. While emerging evidence linked features of ferroptosis induced e.g. by erastin-mediated inhibition of the Xc(-) system or inhibition of glutathione peroxidase 4 (Gpx4) to an increasing number of oxidative cell death paradigms in cancer cells, neurons or kidney cells, the biochemical pathways of oxidative cell death remained largely unclear...
March 9, 2017: Redox Biology
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