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Neurochemistry International

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https://www.readbyqxmd.com/read/28323006/the-role-of-sumoylation-in-cerebral-hypoxia-and-ischemia
#1
REVIEW
Myriam Peters, Betty Wielsch, Johannes Boltze
The process of protein modification by adding or detaching small ubiquitin-like modifiers (SUMO) proteins, called SUMOylation, contributes to the regulation of numerous processes in eukaryotic cells. SUMOylation also represents a key response and adaption mechanism to different forms of metabolic stress. The central nervous system (CNS) and neurons in particular are highly susceptible to hypoxic-ischemic stress due to the lack of significant oxygen and energy reserves. SUMOylation is observed in many molecular responses to metabolic stress in the brain, and is therefore supposed to represent an endogenous neuroprotective mechanism...
March 17, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28315370/control-of-mitochondrial-physiology-and-cell-death-by-the-bcl-2-family-proteins-bax-and-bok
#2
Beatrice D'Orsi, Julia Mateyka, Jochen H M Prehn
Neuronal cell death is often triggered by events that involve intracellular increases in Ca(2+). Under resting conditions, the intracellular Ca(2+) concentration is tightly controlled by a number of extrusion and sequestering mechanisms involving the plasma membrane, mitochondria, and ER. These mechanisms act to prevent a disruption of neuronal ion homeostasis. As these processes require ATP, excessive Ca(2+) overloading may cause energy depletion, mitochondrial dysfunction, and may eventually lead to Ca(2+)-dependent cell death...
March 14, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28302504/mitochondrial-nudix-hydrolases-a-metabolic-link-between-nad-catabolism-gtp-and-mitochondrial-dynamics
#3
Aaron Long, Nina Klimova, Tibor Kristian
NAD(+) catabolism and mitochondrial dynamics are important parts of normal mitochondrial function and are both reported to be disrupted in aging, neurodegenerative diseases, and acute brain injury. While both processes have been extensively studied there has been little reported on how the mechanisms of these two processes are linked. This review focuses on how downstream NAD(+) catabolism via NUDIX hydrolases affects mitochondrial dynamics under pathologic conditions. Additionally, several potential targets in mitochondrial dysfunction and fragmentation are discussed, including the roles of mitochondrial poly(ADP-ribose) polymerase 1(mtPARP1), AMPK, AMP, and intra-mitochondrial GTP metabolism...
March 14, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28300620/catabolism-of-gaba-succinic-semialdehyde-or-gamma-hydroxybutyrate-through-the-gaba-shunt-impair-mitochondrial-substrate-level-phosphorylation
#4
Dora Ravasz, Gergely Kacso, Viktoria Fodor, Kata Horvath, Vera Adam-Vizi, Christos Chinopoulos
GABA is catabolized in the mitochondrial matrix through the GABA shunt, encompassing transamination to succinic semialdehyde followed by oxidation to succinate by the concerted actions of GABA transaminase (GABA-T) and succinic semialdehyde dehydrogenase (SSADH), respectively. Gamma-hydroxybutyrate (GHB) is a neurotransmitter and a psychoactive drug that could enter the citric acid cycle through transhydrogenation with α-ketoglutarate to succinic semialdehyde and d-hydroxyglutarate, a reaction catalyzed by hydroxyacid-oxoacid transhydrogenase (HOT)...
March 11, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28286208/oxoisoaporphine-alkaloid-derivative-8-1-reduces-a%C3%AE-1-42-secretion-and-toxicity-in-human-cell-and-caenorhabditis-elegans-models-of-alzheimer-s-disease
#5
Liyingzi Huang, Yunfeng Luo, Zhijun Pu, Xianghui Kong, Xiang Fu, Huanhuan Xing, Shenqi Wei, Huang Tang, Wei Chen
Alzheimer's disease (AD) is a multifactorial neurodegenerative disease and a growing health problem worldwide. Because the drugs currently used to treat AD have certain drawbacks such as single targeting, there is a need to develop novel multi-target compounds, among which oxoisoaporphine alkaloid derivatives are promising candidates. In this study, the possible anti-AD activities of 14 novel oxoisoaporphine alkaloid derivatives that we synthesized were screened and evaluated. We found that, in the 14 novel derivatives, compound 8-1 significantly reduced Aβ1-42 secretion in SH-SY5Y cells overexpressing the Swedish mutant form of human β-amyloid precursor protein (APPsw)...
March 9, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28284975/chronic-treatment-with-taurine-after-intracerebroventricular-streptozotocin-injection-improves-cognitive-dysfunction-in-rats-by-modulating-oxidative-stress-cholinergic-functions-and-neuroinflammation
#6
K H Reeta, Devendra Singh, Y K Gupta
The present study investigated the neuroprotective effects of taurine, an essential amino acid for growth and development of central nervous system. Intracerebroventricular streptozotocin (ICV-STZ) model of cognitive impairment was used in male Wistar rats (270 ± 20 g). Morris water maze, elevated plus maze and passive avoidance paradigm were used to assess cognitive performance. Taurine (40, 60 and 120 mg/kg) was administered orally for 28 days following STZ administration on day 1. Oxidative stress parameters (malondialdehyde, glutathione, nitric oxide and superoxide dismutase) and cholinesterases (acetylcholinesterase and butyrylcholinesterase) activity were measured at end of the study in the cortex and hippocampus...
March 8, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28284974/mevalonolactone-disrupts-mitochondrial-functions-and-induces-permeability-transition-pore-opening-in-rat-brain-mitochondria-implications-for-the-pathogenesis-of-mevalonic-aciduria
#7
Cristiane Cecatto, Alexandre Umpierrez Amaral, Janaína Camacho da Silva, Alessandro Wajner, Kálita Dos Santos Godoy, Rafael Teixeira Ribeiro, Aline de Mello Gonçalves, Carmen Regla Vargas, Moacir Wajner
Mevalonic aciduria (MVA) is caused by severe deficiency of mevalonic kinase activity leading to tissue accumulation and high urinary excretion of mevalonic acid (MA) and mevalonolactone (ML). Patients usually present severe neurologic symptoms whose pathophysiology is poorly known. Here, we tested the hypothesis that the major accumulating metabolites are toxic by investigating the in vitro effects of MA and ML on important mitochondrial functions in rat brain and liver mitochondria. ML, but not MA, markedly decreased mitochondrial membrane potential (ΔΨm), NAD(P)H content and the capacity to retain Ca(2+) in the brain, besides inducing mitochondrial swelling...
March 8, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28279752/novel-spiroimidazopyridine-derivative-sak3-improves-methimazole-induced-cognitive-deficits-in-mice
#8
Husain Noreen, Yasushi Yabuki, Kohji Fukunaga
Methimazole (MMI) is a first-line therapy used to manage hyperthyroidism and Graves' disease. Despite its therapeutic benefit, chronic MMI administration can lead to hypothyroidism and perturb brain homeostasis in patients, resulting in neuropsychiatric disorders such as depression and cognitive dysfunction. We recently developed the spiroimidazopyridine derivative SAK3 as cognitive enhancer; however, mechanisms underlying its activity remained unclear. Here, we show that SAK3 potentially improves cognitive impairment seen following MMI-induced hypothyroidism...
March 6, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28279751/blockade-of-ccr5-receptor-prevents-m2-microglia-phenotype-in-a-microglia-glioma-paradigm
#9
Emilia Laudati, Diego Currò, Pierluigi Navarra, Lucia Lisi
Microglia express chemokines and their cognate receptors that were found to play important roles in many processes required for tumor development, such as tumor growth, proliferation, invasion, and angiogenesis. Among the chemokine receptor, CCR5 have been documented in different cancer models; in particular, CCR5 is highly expressed in human glioblastoma, where it is associated to poor prognosis. In the present study, we investigated the effect of CCR5 receptor blockade on a paradigm of microglia-glioma interaction; the CCR5 blocker maraviroc (MRV) was used as a pharmacological tool...
March 6, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28279750/neurons-and-astrocytes-in-an-infantile-neuroaxonal-dystrophy-inad-mouse-model-show-characteristic-alterations-in-glutamate-induced-ca-2-signaling
#10
Mikhail Strokin, Georg Reiser
INAD (infantile neuroaxonal dystrophy, OMIM#256600), an autosomal recessive inherited degenerative disease, is associated with PLA2G6 mutations. PLA2G6 encodes Ca(2+)-independent phospholipase A2 (VIA iPLA2). However, it is unclear how the PLA2G6-mutations lead to disease. Non-canonical functions, which were suggested for VIA iPLA2, such as regulation of cellular and mitochondrial Ca(2+) are promising candidates. Therefore, we investigate glutamate (Glu)-evoked Ca(2+) signals in neurons and astrocytes in co-culture obtained from three INAD mouse model strains with Pla2g6 mutations, (i) hypomorphic Pla2g6 allele with reduced transcript levels, (ii) knocked-out Pla2g6, and (iii) (G373R)-point mutation with inactive VIA iPLA2 enzyme...
March 6, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28268188/-1-h-nmr-based-metabolomics-reveals-neurochemical-alterations-in-the-brain-of-adolescent-rats-following-acute-methylphenidate-administration
#11
Emmanuel Quansah, Victor Ruiz-Rodado, Martin Grootveld, Fay Probert, Tyra S C Zetterström
The psychostimulant methylphenidate (MPH) is increasingly used in the treatment of attention deficit hyperactivity disorder (ADHD). While there is little evidence for common brain pathology in ADHD, some studies suggest a right hemisphere dysfunction among people diagnosed with the condition. However, in spite of the high usage of MPH in children and adolescents, its mechanism of action is poorly understood. Given that MPH blocks the neuronal transporters for dopamine and noradrenaline, most research into the effects of MPH on the brain has largely focused on these two monoamine neurotransmitter systems...
March 6, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28257830/neuroprotective-effects-of-a-novel-peptide-fk18-under-oxygen-glucose-deprivation-in-sh-sy5y-cells-and-retinal-ischemia-in-rats%C3%A2-via%C3%A2-the-akt-pathway
#12
Shuyu Xiong, Yupeng Xu, Mingming Ma, Haiyan Wang, Fang Wei, Qing Gu, Xun Xu
Ischemic neuronal injury is associated with several life- and vision-threatening diseases. Neuroprotection is essential in the treatment of these diseases. Here, we identified and characterized a novel peptide, FK18, from basic fibroblast growth factor (bFGF). We further assessed the neuroprotective effects of this peptide and its potential mechanisms using the in vitro oxygen-glucose deprivation (OGD) model in SH-SY5Y cells and the in vivo retinal ischemia-reperfusion (I/R) injury model to mimic ischemic neuronal injury...
February 28, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28245997/contrasting-roles-of-immune-cells-in-tissue-injury-and-repair-in-stroke-the-dark-and-bright-side-of-immunity-in-the-brain
#13
REVIEW
Aditya Rayasam, Martin Hsu, Gianna Hernández, Julie Kijak, Anders Lindstedt, Christian Gerhart, Matyas Sandor, Zsuzsanna Fabry
Despite considerable efforts in research and clinical studies, stroke is still one of the leading causes of death and disability worldwide. Originally, stroke was considered a vascular thrombotic disease without significant immune involvement. However, over the last few decades it has become increasingly obvious that the immune responses can significantly contribute to both tissue injury and protection following stroke. Recently, much research has been focused on the immune system's role in stroke pathology and trying to elucidate the mechanism used by immune cells in tissue injury and protection...
February 25, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28242245/inhibition-of-neuronal-mitochondrial-complex-i-or-lysosomal-glucocerebrosidase-is-associated-with-increased-dopamine-and-serotonin-turnover
#14
Carmen de la Fuente, Derek Burke, Simon Eaton, Simon J Heales
Parkinson's disease (PD) is a neurodegenerative disorder caused by loss of dopaminergic and serotoninergic signalling. A number of pathogenic mechanisms have been implicated including loss of mitochondrial function at the level of complex I, and lysosomal metabolism at the level of lysosomal glucocerebrosidase (GBA1). In order to investigate further the potential involvement of complex I and GBA1 in PD, we assessed the impact of loss of respective enzyme activities upon dopamine and serotonin turnover. Using SH-SY5Y cells, complex I deficiency was modelled by using rotenone whilst GBA1 deficiency was modelled by the use of conduritol B epoxide (CBE)...
February 24, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28237844/characterization-of-the-cystine-glutamate-antiporter-in-cultured-bergmann-glia-cells
#15
Edna Suárez-Pozos, Zila Martínez-Lozada, Orquidia G Méndez-Flores, Alain M Guillem, Luisa C Hernández-Kelly, Francisco Castelán, Tatiana N Olivares-Bañuelos, Donaji Chi-Castañeda, Mustapha Najimi, Arturo Ortega
Glutamate, the major excitatory transmitter in the vertebrate brain is a potent neurotoxin through the over-stimulation of its specific membrane receptors. In accordance, a tight regulation of its extracellular levels by plasma membrane transporters is present. A family of excitatory amino acid transporters is expressed in neurons and glia cells and is responsible of the removal of the neurotransmitter from the synaptic cleft. Glial transporters account for more than 80% of the brain uptake activity. The cystine/glutamate antiporter is another plasma membrane-bound protein critically involved in glutamatergic transmission...
February 24, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28237843/characterization-of-energy-and-neurotransmitter-metabolism-in-cortical-glutamatergic-neurons-derived-from-human-induced-pluripotent-stem-cells-a-novel-approach-to-study-metabolism-in-human-neurons
#16
Blanca I Aldana, Yu Zhang, Maria Fog Lihme, Lasse K Bak, Jørgen E Nielsen, Bjørn Holst, Poul Hyttel, Kristine K Freude, Helle S Waagepetersen
Alterations in the cellular metabolic machinery of the brain are associated with neurodegenerative disorders such as Alzheimer's disease. Novel human cellular disease models are essential in order to study underlying disease mechanisms. In the present study, we characterized major metabolic pathways in neurons derived from human induced pluripotent stem cells (hiPSC). With this aim, cultures of hiPSC-derived neurons were incubated with [U-(13)C]glucose, [U-(13)C]glutamate or [U-(13)C]glutamine. Isotopic labeling in metabolites was determined using gas chromatography coupled to mass spectrometry, and cellular amino acid content was quantified by high-performance liquid chromatography...
February 24, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28238791/selol-an-organic-selenium-donor-prevents-lipopolysaccharide-induced-oxidative-stress-and-inflammatory-reaction-in-the-rat-brain
#17
Agnieszka Dominiak, Anna Wilkaniec, Henryk Jęśko, Grzegorz A Czapski, Anna M Lenkiewicz, Eliza Kurek, Piotr Wroczyński, Agata Adamczyk
Neuroinflammation and oxidative stress are key intertwined pathological factors in many neurological, particularly neurodegenerative diseases, such as Alzheimer's and Parkinson's disorders as well as autism. The present study was conducted to evaluate the protective effects of Selol, an organic selenium donor, against lipopolysaccharide (LPS)-mediated inflammation in rat brain. The results demonstrated that the peripheral administration of LPS in a dose of 100 μg/kg b.w. evoked typical pathological reaction known as systemic inflammatory response...
February 23, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28238790/multifunctional-liposomes-interact-with-abeta-in-human-biological-fluids-therapeutic-implications-for-alzheimer-s-disease
#18
Elisa Conti, Maria Gregori, Isabella Radice, Fulvio Da Re, Denise Grana, Francesca Re, Elisa Salvati, Massimo Masserini, Carlo Ferrarese, Chiara Paola Zoia, Lucio Tremolizzo
The accumulation of extracellular amyloid beta (Abeta42) both in brain and in cerebral vessels characterizes Alzheimer's disease (AD) pathogenesis. Recently, the possibility to functionalize nanoparticles (NPs) surface with Abeta42 binding molecules, making them suitable tools for reducing Abeta42 burden has been shown effective in models of AD. Aim of this work consisted in proving that NPs might be effective in sequestering Abeta42 in biological fluids, such as CSF and plasma. This demonstration is extremely important considering that these Abeta42 pools are in continuum with the brain parenchyma with drainage of Abeta from interstitial brain tissue to blood vessel and plasma...
February 23, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28235551/mitophagy-in-neurodegeneration-and-aging
#19
REVIEW
Elayne M Fivenson, Sofie Lautrup, Nuo Sun, Morten Scheibye-Knudsen, Tinna Stevnsner, Hilde Nilsen, Vilhelm A Bohr, Evandro F Fang
Mitochondrial dysfunction contributes to normal aging and a wide spectrum of age-related diseases, including neurodegenerative disorders such as Parkinson's disease and Alzheimer's disease. It is important to maintain a healthy mitochondrial population which is tightly regulated by proteolysis and mitophagy. Mitophagy is a specialized form of autophagy that regulates the turnover of damaged and dysfunctional mitochondria, organelles that function in producing energy for the cell in the form of ATP and regulating energy homeostasis...
February 21, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28232070/downregulation-of-mfn2-participates-in-manganese-induced-neuronal-apoptosis-in-rat-striatum-and-pc12-cells
#20
Xinhang Liu, Jianbin Yang, Chunhua Lu, Shengyang Jiang, Xiaoke Nie, Jingling Han, Lifeng Yin, Junkang Jiang
Manganese (Mn) is a widely distributed trace element that is essential for normal brain function and development. However, chronic exposure to excessive Mn has been known to lead to neuronal loss and manganism, a disease with debilitating motor and cognitive deficits, whose clinical syndrome resembling idiopathic Parkinson's disease (IPD). However, the precise molecular mechanism underlying Mn neurotoxicity remains largely unclear. Accumulating evidence indicates that abnormal mitochondrial functionality is an early and causal event in Mn-induced neurodegeneration and apoptosis...
February 21, 2017: Neurochemistry International
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