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Neurochemistry International

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https://www.readbyqxmd.com/read/28711656/upregulation-of-cdh1-signaling-in-the-hippocampus-attenuates-brain-damage-after-transient-global-cerebral-ischemia-in-rats
#1
Bo Zhang, Kai Wei, Xuan Li, Rong Hu, Jin Qiu, Yue Zhang, Wenlong Yao, Chuanhan Zhang, Chang Zhu
Cerebral ischemia is a major cause of brain dysfunction. The E3 ubiquitin ligase anaphase-promoting complex and its coactivator Cdh1 have been reported to be involved in the regulation of neuronal survival, differentiation, axonal growth and synaptic development in the central nervous system. However, its role in the ischemic brain and the underlying mechanisms remain poorly understood. The present study aimed to investigate the effects of Cdh1 overexpression on the ischemic rat brain by direct intra-hippocampal injection of lentivirus-delivered Cdh1 before transient global cerebral ischemia reperfusion...
July 12, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28711655/ubiquitination-at-the-mitochondria-in-neuronal-health-and-disease
#2
REVIEW
Christian Covill-Cooke, Jack Howden, Nicol Birsa, Josef Kittler
The preservation of mitochondrial function is of particular importance in neurons given the high energy requirements of action potential propagation and synaptic transmission. Indeed, disruptions in mitochondrial dynamics and quality control are linked to cellular pathology in neurodegenerative diseases, such as Alzheimer's and Parkinson's disease. Here, we will discuss the role of ubiquitination by the E3 ligases: Parkin, MARCH5 and Mul1, and how they regulate mitochondrial homeostasis. Furthermore, given the role of Parkin and Mul1 in the formation of mitochondria-derived vesicles we give an overview of this area of mitochondrial homeostasis...
July 12, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28711654/involvement-of-endoplasmic-reticulum-stress-and-neurite-outgrowth-in-the-model-mice-of-autism-spectrum-disorder
#3
Koichi Kawada, Seisuke Mimori, Yasunobu Okuma, Yasuyuki Nomura
Neurodevelopmental disorders are congenital impairments, impeding the growth and development of the central nervous system. These disorders include autism spectrum disorder (ASD) and attention-deficit/hyperactivity disorder in Diagnostic and Statistical Manual of Mental Disorders-5. ASD is caused by a gene defect and chromosomal duplication. Despite numerous reports on ASD, the pathogenic mechanisms are not clear. The optimal methods to prevent ASD and to treat it are also not clear. Other studies have reported that endoplasmic reticulum (ER) stress contributes to the pathogenesis of neurodegenerative diseases...
July 12, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28697973/traffic-jam-hypothesis-relationship-between-endocytic-dysfunction-and-alzheimer-s-disease
#4
REVIEW
Nobuyuki Kimura, Katsuhiko Yanagisawa
Membrane trafficking pathways, like the endocytic pathway, carry out fundamental cellular processes that are essential for normal functioning. One such process is regulation of cell surface receptor signaling. A growing body of evidence suggests that β-amyloid protein (Aβ) plays a key role in Alzheimer's disease (AD) pathogenesis. Cleavage of Aβ from its precursor, β-amyloid precursor protein (APP), occurs through the endocytic pathway in neuronal cells. In early-stage AD, intraneuronal accumulation of abnormally enlarged endosomes is common, indicating that endosome trafficking is disrupted...
July 8, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28697972/neuroprotection-of-edaravone-on-the-hippocampus-of-kainate-induced-epilepsy-rats-through-nrf2-ho-1-pathway
#5
Zhiguang Liu, Chengzhi Yang, Xinyan Meng, Zaili Li, Cunling Lv, Peiwei Cao
Epilepsy is a severe and chronic neurological disease. Edaravone is an effective free radical scavenger and has been reported to prevent neuronal loss induced by Kainate (KA). However, the molecular mechanisms by which edaravone inhibits KA-induced neuron injury remain elusive. Seventy adult male Wistar rats were randomly divided into 7 groups. For KA treatment, Kainate (4 μg/kg) were administrated in the right hippocampus CA3 region with sereotactic technique. And for edaravone treatment, the rats were intraperitoneal injection with edaravone (10 mg kg (- 1) d (- 1))...
July 8, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28687401/pathophysiological-role-of-prostaglandin-e2-induced-up-regulation-of-the-ep2-receptor-in-motor-neuron-like-nsc-34-cells-and-lumbar-motor-neurons-in-als-model-mice
#6
Yasuhiro Kosuge, Hiroko Miyagishi, Yuki Yoneoka, Keiko Yoneda, Hiroshi Namgo, Kumiko Ishige, Yoshihisa Ito
Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease characterized by selective degeneration of motor neurons. The primary triggers for motor neuronal death are still unknown, but inflammation is considered to be an important factor contributing to the pathophysiology of ALS both clinically and in ALS models. Prostaglandin E2 (PGE2) and its corresponding four E-prostanoid receptors play a pivotal role in the degeneration of motor neurons in human and transgenic models of ALS. It has also been shown that PGE2-EP2 signaling in glial cells (astrocytes or microglia) promotes motor neuronal death in G93A mice...
July 4, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28668471/the-broad-spectrum-of-signaling-pathways-regulated-by-unfolded-protein-response-in-neuronal-homeostasis
#7
REVIEW
Atsushi Saito, Kazunori Imaizumi
The protein folding capabilities in the endoplasmic reticulum (ER) are disturbed by alternations in the cellular homeostasis such as the disruption of calcium ion homeostasis, the expression of mutated proteins and oxidative stress. In response to these ER dysfunctions, eukaryotic cells activate canonical branches of signal transduction cascades to restore the protein folding capacity and avoid irreversible damages, collectively termed the unfolded protein response (UPR). Prolonged ER dysfunctions and the downregulation of UPR signaling pathways have been accepted as a crucial trigger for the pathogenesis of various neurodegenerative diseases...
June 28, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28652220/inhibition-of-alzheimer-s-amyloid-beta-aggregation-in-vitro-by-carbenoxolone-insight-into-mechanism-of-action
#8
Sheetal Sharma, Bimla Nehru, Avneet Saini
BACKGROUND: The major hallmark of Alzheimer's disease (AD) is the formation of amyloid aggregates, which are formed due to improper folding of proteins leading to the aggregation of amyloid beta (Aβ) 42 peptide. Inhibition of Aβ 42 aggregation using a drug such as carbenoxolone (Cbx), which has already been stated as neuroprotective, appears to be an effective approach against AD. OBJECTIVE: The present study was designed to investigate the anti-fibrillation activity of Cbx against the Aβ 42 aggregation...
June 24, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28647375/type-i-interferon-signalling-through-ifnar1-plays-a-deleterious-role-in-the-outcome-after-stroke
#9
Moses Zhang, Catherine E Downes, Connie H Y Wong, Kate M Brody, Pedro L Guio-Agulair, Jodee Gould, Robert Ates, Paul J Hertzog, Juliet M Taylor, Peter J Crack
Neuroinflammation contributes significantly to the pathophysiology of stroke. Here we test the hypothesis that the type I interferon receptor (IFNAR1) plays a critical role in neural injury after stroke by regulating the resultant pro-inflammatory environment. Wild-type and IFNAR1(-/-) primary murine neurons and glia were exposed to oxygen glucose deprivation (OGD) and cell viability was assessed. Transient cerebral ischemia/reperfusion injury was induced by mid-cerebral artery occlusion (MCAO) in wild-type and IFNAR1(-/-) and IFNAR2(-/-) mice in vivo, and infarct size, and molecular parameters measured...
June 22, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28647376/mitochondrial-permeability-transition-pore-back-to-the-drawing-board
#10
Christos Chinopoulos
Current models theorizing on what the mitochondrial permeability transition (mPT) pore is made of, implicate the c-subunit rings of ATP synthase complex. However, two very recent studies, one on atomistic simulations and in the other disrupting all genes coding for the c subunit disproved those models. As a consequence of this, the structural elements of the pore remain unknown. The purpose of the present short-review is to (i) briefly review the latest findings, (ii) serve as an index for more comprehensive reviews regarding mPT specifics, (iii) reiterate on the potential pitfalls while investigating mPT in conjunction to bioenergetics, and most importantly (iv) suggest to those in search of mPT pore identity, to also look elsewhere...
June 21, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28629771/chemokines-play-complex-roles-in-cerebral-ischemia
#11
REVIEW
Chen Chen, Shi-Feng Chu, Dan-Dan Liu, Zhao Zhang, Ling-Lei Kong, Xin Zhou, Nai-Hong Chen
Ischemic stroke (IS) is a disease caused by deficiency of blood and oxygen in focal or complete brain, followed by inflammation cascade and other pathological reactions, which finally lead to irreversible damage to the cerebrum. For the inflammation is a key progress at the initiation of ischemia and poststroke, and chemokines work as vital cytokines in inflammation, we focus the roles of chemokines in IS. Studies have shown cerebral ischemia is associated with marked induction of both CXC and CC chemokines which resulting in extensive leukocyte infiltration in the ischemic brain, and neutrophil infiltration may increase cerebral edema inducing injury in the ischemic area...
June 16, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28627367/nrf2-pathway-activation-upon-rotenone-treatment-in-human-ipsc-derived-neural-stem-cells-undergoing-differentiation-towards-neurons-and-astrocytes
#12
Francesca Pistollato, David Canovas-Jorda, Dimitra Zagoura, Anna Bal-Price
Activation of Nrf2/ARE signaling pathway occurs ubiquitously in most cell types upon induction of oxidative stress. Rotenone, an inhibitor of mitochondrial complex I, can be used to trigger oxidative stress, stimulate the activation of Nrf2 pathway in neuronal and astrocytic cells and assess neurotoxicity. We have previously demonstrated that an acute treatment with rotenone can induce Nrf2 activation, which leads to astrocyte activation and dopaminergic (DA) neuronal cell death in a mixed neuronal/astrocytic cell model derived from human induced pluripotent stem cells (hiPSCs)...
June 13, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28627366/pqbp1-an-intrinsically-disordered-denatured-protein-at-the-crossroad-of-intellectual-disability-and-neurodegenerative-diseases
#13
REVIEW
Hitoshi Okazawa
PQBP1 (polyglutamine binding protein-1) is the earliest identified molecule among the group of disease-related intrinsically disordered/denatured proteins. PQBP1 interacts with splicing-related factors via the disordered/denatured domain and regulates post-transcriptional gene expression. The mutations cause intellectual disability due to decreased dendritic spines and abnormal expression of synapse molecules in neurons, and microcephaly due to elongated cell cycle time and abnormal expression of cell cycle proteins in neural stem progenitor cells...
June 13, 2017: Neurochemistry International
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
#14
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/28606823/alpha-lipoic-acid-attenuates-acute-neuroinflammation-and-long-term-cognitive-impairment-after-polymicrobial-sepsis
#15
Amanda Della Giustina, Mariana Pereira Goldim, Lucinéia Gainski Danielski, Drielly Florentino, Khiany Mathias, Leandro Garbossa, Aloir Neri Oliveira Junior, Maria Eduarda Fileti, Graciela Freitas Zarbato, Naiana da Rosa, Ana Olívia Martins Laurentino, Jucélia Jeremias Fortunato, Francielle Mina, Tatiani Bellettini-Santos, Josiane Budni, Tatiana Barichello, Felipe Dal-Pizzol, Fabricia Petronilho
Sepsis is a complication of an infection which imbalance the normal regulation of several organ systems, including the central nervous system (CNS). Evidence points towards inflammation and oxidative stress as major steps associated with brain dysfunction in sepsis. Thus, we investigated the α-lipoic acid (ALA) effect as an important antioxidant compound on brain dysfunction in rats. Wistar rats were subjected to sepsis by cecal ligation and perforation (CLP) or sham (control) and treated orally with ALA (200 mg/kg after CLP) or vehicle...
June 10, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28606822/genistein-a-dietary-soy-isoflavone-exerts-antidepressant-like-effects-in-mice-involvement-of-serotonergic-system
#16
Pei Hu, Li Ma, Yan-Gui Wang, Feng Ye, Chuang Wang, Wen-Hua Zhou, Xin Zhao
Genistein, a principal isoflavone property of soybeans, possesses multiple pharmacological activities such as neuroprotection. Recently, it was reported that genistein exerted antidepressant-like effects in animal models, but the mechanism of action remains ambiguous. The purpose of this study was to investigate the antidepressant-like effect of genistein in mice and explore the underlying mechanism(s), using two mouse models of depression, i.e. forced swim test (FST) and tail suspension test (TST). Chronic, but not acute (single dose), genistein treatment (5, 15 or 45 mg/kg, p...
June 9, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28603024/functional-research-and-molecular-mechanism-of-kainic-acid-induced-denitrosylation-of-thioredoxin-1-in-rat-hippocampus
#17
Hongning Yang, Ningjun Zhao, Lanxin Lv, Xianliang Yan, Shuqun Hu, Tie Xu
Thioredoxin-1 (Trx1) has long been recognized as a redox regulator, and is implicated in the inhibition of cell apoptosis. Trx1 is essential for the maintenance of the S-nitrosylation of molecules in cells. The S-nitrosylation of Trx1 is essential for the physiological function such as preservation of the redox regulatory activity. The mechanisms underlying Trx1 denitrosylation induced by kainate acid (KA) injection still remain uncharacterized. Our results showed that the S-nitrosylation levels of Trx1 were decreased subsequent to KA injection and that the glutamate receptor 6 (GluR6) antagonist NS102 could inhibit the denitrosylation of Trx1...
June 8, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28600187/vascular-endothelial-growth-factor-influences-migration-and-focal-adhesions-but-not-proliferation-or-viability-of-human-neural-stem-progenitor-cells-derived-from-olfactory-epithelium
#18
Gerardo Bernabé Ramírez-Rodríguez, Gerardo Rodrigo Perera-Murcia, Leonardo Ortiz-López, Nelly Maritza Vega-Rivera, Harish Babu, Maria García-Anaya, Jorge Julio González-Olvera
In humans, new neurons are continuously added in the olfactory epithelium even in the adulthood. The resident neural stem/progenitor cells (hNS/PCs-OE) in the olfactory epithelium are influenced by several growth factors and neurotrophins. Among these modulators the vascular endothelial growth factor (VEGF) has attracted attention due its implicated in cell proliferation, survival and migration of other type of neural/stem progenitor cells. Interestingly, VEGFr2 receptor expression in olfactory epithelium has been described in amphibians but not in humans...
June 7, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28579060/human-dihydrolipoamide-dehydrogenase-e3-deficiency-novel-insights-into-the-structural-basis-and-molecular-pathomechanism
#19
REVIEW
Attila Ambrus, Vera Adam-Vizi
This review summarizes our present view on the molecular pathogenesis of human (h) E3-deficiency caused by a variety of genetic alterations with a special emphasis on the moonlighting biochemical phenomena related to the affected (dihydro)lipoamide dehydrogenase (LADH, E3, gene: dld), in particular the generation of reactive oxygen species (ROS). E3-deficiency is a rare autosomal recessive genetic disorder frequently presenting with a neonatal onset and premature death; the highest carrier rate of a single pathogenic dld mutation (1:94-1:110) was found among Ashkenazi Jews...
June 2, 2017: Neurochemistry International
https://www.readbyqxmd.com/read/28579059/neuroketotherapeutics-a-modern-review-of-a-century-old-therapy
#20
REVIEW
Scott J Koppel, Russell H Swerdlow
Neuroketotherapeutics represent a class of bioenergetic medicine therapies that feature the induction of ketosis. These therapies include medium-chain triglyceride supplements, ketone esters, fasting, strenuous exercise, the modified Atkins diet, and the classic ketogenic diet. Extended experience reveals persons with epilepsy, especially pediatric epilepsy, benefit from ketogenic diets although the mechanisms that underlie its effects remain unclear. Data indicate ketotherapeutics enhance mitochondrial respiration, promote neuronal long-term potentiation, increase BDNF expression, increase GPR signaling, attenuate oxidative stress, reduce inflammation, and alter protein post-translational modifications via lysine acetylation and β-hydroxybutyrylation...
June 1, 2017: Neurochemistry International
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