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Journal of Neurochemistry

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https://www.readbyqxmd.com/read/28643372/fine-tuning-perk-signaling-for-neuroprotection
#1
REVIEW
Mark Halliday, Daniel Hughes, Giovanna Mallucci
Protein translation and folding are tightly controlled processes in all cells, by proteostasis, an important component of which is the unfolded protein response (UPR). During periods of endoplasmic reticulum stress due to protein misfolding, the UPR activates a coordinated response in which the PERK branch activation restricts translation, while a variety of genes involved with protein folding, degradation, chaperone expression and stress responses are induced through signaling of the other branches. Chronic overactivation of the UPR, particularly the PERK branch is observed in the brains of patients in a number of protein misfolding neurodegenerative diseases, including Alzheimer's, and Parkinson's diseases and the taopathies...
June 23, 2017: Journal of Neurochemistry
https://www.readbyqxmd.com/read/28640985/the-interaction-between-progranulin-and-prosaposin-is-mediated-by-granulins-and-the-linker-region-between-saposin-b-and-c
#2
Xiaolai Zhou, Peter M Sullivan, Lirong Sun, Fenghua Hu
The frontotemporal lobar degeneration (FTLD) protein progranulin (PGRN) is essential for proper lysosomal function. PGRN localizes in the lysosomal compartment within the cell. Prosaposin (PSAP), the precursor of lysosomal saposin activators (saposin A, B, C, D), physically interacts with PGRN. Previously we have shown that PGRN and PSAP facilitate each other's lysosomal trafficking. Here we report that the interaction between PSAP and PGRN requires the linker region of saposin B and C (BC linker). PSAP protein with the BC linker mutated fails to interact with PGRN and target PGRN to lysosomes in the biosynthetic and endocytic pathways...
June 22, 2017: Journal of Neurochemistry
https://www.readbyqxmd.com/read/28640931/ischemia-responsive-protein-94-is-a-key-mediator-of-ischemic-neuronal-injury-induced-microglial-activation
#3
Rajiv Tikamdas, Sarthak Singhal, Ping Zhang, Justin A Smith, Eric G Krause, Stanley M Stevens, Sihong Song, Bin Liu
Neuroinflammation, especially activation of microglia, the key immune cells in the brain, has been proposed to contribute to the pathogenesis of ischemic stroke. However, the dynamics and the potential mediators of microglial activation following ischemic neuronal injury are not well understood. In this study, using oxygen/glucose deprivation and reoxygenation (OGD/R) with neuronal and microglial cell cultures as an in vitro model of ischemic neuronal injury, we set out to identify neuronal factors released from injured neurons that are capable of inducing microglial activation...
June 22, 2017: Journal of Neurochemistry
https://www.readbyqxmd.com/read/28632969/vegf-is-neuroprotective-against-ischemic-brain-injury-by-inhibiting-scavenger-receptor-a-expression-on-microglia
#4
Zheng Xu, Kaiwei Han, Jigang Chen, Chunhui Wang, Yan Dong, Mingkun Yu, Rulin Bai, Chenguang Huang, Lijun Hou
Vascular endothelial growth factor (VEGF) is a secreted mitogen associated with angiogenesis. VEGF has long been thought to be a potent neurotrophic factor for the survival of spinal cord neuron. However, the role of VEGF in the regulation of ischemic brain injury remains unclear. In the study rats were subjected to MCAO (middle cerebral artery occlusion) followed by intraperitoneal injection of VEGF165 (10 mg/kg) immediately after surgery and once daily till the day 10, and the expression of target genes was assayed using qPCR, western blot and immunofluorescence, and the role of VEGF165 in regulating ischemic brain injury was assayed...
June 20, 2017: Journal of Neurochemistry
https://www.readbyqxmd.com/read/28632947/pimozide-reduces-toxic-forms-of-tau-in-tauc3-mice-via-ampk-mediated-autophagy
#5
YoungDoo Kim, Eun Il Jeong, Jihoon Nah, Seung-Min Yoo, WonJae Lee, Youbin Kim, Seowon Moon, Se-Hoon Hong, Yong-Keun Jung
In neurodegenerative diseases like Alzheimer's disease (AD), tau is hyperphosphorylated and forms aggregates and neurofibrillary tangles in affected neurons. Autophagy is critical to clear the aggregates of disease-associated proteins and is often altered in patients and animal models of AD. Because mTOR (mechanistic target of rapamycin) negatively regulates autophagy and is hyperactive in the brains of patients with AD, mTOR is an attractive therapeutic target for AD. However, pharmacological strategies to increase autophagy by targeting mTOR inhibition cause various side effects...
June 20, 2017: Journal of Neurochemistry
https://www.readbyqxmd.com/read/28632905/the-malleable-brain-plasticity-of-neural-circuits-and-behavior-a-review-from-students-to-students
#6
REVIEW
Natascha Schaefer, Carola Rotermund, Eva-Maria Blumrich, Mychael V Lourenco, Pooja Joshi, Regina U Hegemann, Sumit Jamwal, Nilufar Ali, Ezra Michelet García Romero, Sorabh Sharma, Shampa Ghosh, Jitendra K Sinha, Hannah Loke, Vishal Jain, Katarzyna Lepeta, Ahmad Salamian, Mahima Sharma, Mojtaba Golpich, Katarzyna Nawrotek, Ramesh K Paidi, Sheila M Shahidzadeh, Tetsade Piermartiri, Elham Amini, Veronica Pastor, Yvette Wilson, Philip A Adeniyi, Ashok K Datusalia, Benham Vafadari, Vedangana Saini, Edna Suárez-Pozos, Neetu Kushwah, Paula Fontanet, Anthony J Turner
One of the most intriguing features of the brain is its ability to be malleable, allowing it to adapt continually to changes in the environment. Specific neuronal activity patterns drive long-lasting increases or decreases in the strength of synaptic connections, referred to as long-term potentiation (LTP) and long-term depression (LTD) respectively. Such phenomena have been described in a variety of model organisms, which are used to study molecular, structural, and functional aspects of synaptic plasticity...
June 20, 2017: Journal of Neurochemistry
https://www.readbyqxmd.com/read/28628228/epigenetic-mechanisms-underlying-nmda-receptor-hypofunction-in-the-prefrontal-cortex-of-juvenile-animals-in-the-mam-model-for-schizophrenia
#7
Yelena Gulchina, Song-Jun Xu, Melissa A Snyder, Felice Elefant, Wen-Jun Gao
Schizophrenia (SCZ) is characterized not only by psychosis, but also by working memory and executive functioning deficiencies, processes that rely on the prefrontal cortex (PFC). Because these cognitive impairments emerge prior to psychosis onset, we investigated synaptic function during development in the neurodevelopmental methylazoxymethanol acetate (MAM) model for SCZ. Specifically, we hypothesize that NMDAR hypofunction is attributable to reductions in the NR2B subunit through aberrant epigenetic regulation of gene expression, resulting in deficient synaptic physiology and PFC-dependent cognitive dysfunction, a hallmark of SCZ...
June 19, 2017: Journal of Neurochemistry
https://www.readbyqxmd.com/read/28628214/unconventional-role-of-voltage-gated-proton-channels-vsop-hv1-in-regulation-of-microglial-ros-production
#8
Takafumi Kawai, Yoshifumi Okochi, Tomohiko Ozaki, Yoshio Imura, Schuichi Koizumi, Maya Yamazaki, Manabu Abe, Kenji Sakimura, Toshihide Yamashita, Yasushi Okamura
It has been established that voltage-gated proton channels (VSOP/Hv1), encoded by Hvcn1, support reactive oxygen species (ROS) production in phagocytic activities of neutrophils (El Chemaly et al. 2010) and antibody production in B lymphocytes (Capasso et al. 2010). VSOP/Hv1 is a potential therapeutic target for brain ischemia, since Hvcn1 deficiency reduces microglial ROS production and protects brain from neuronal damage (Wu et al. 2012). In the present study, we report that VSOP/Hv1 has paradoxical suppressive role in ROS production in microglia...
June 19, 2017: Journal of Neurochemistry
https://www.readbyqxmd.com/read/28628213/changes-in-kynurenine-pathway-metabolism-in-parkinson-patients-with-l-dopa-induced-dyskinesia
#9
Jesper F Havelund, Andreas D Andersen, Michael Binzer, Morten Blaabjerg, Niels H H Heegaard, Egon Stenager, Nils J Faergeman, Jan Bert Gramsbergen
L-DOPA is the most effective drug in the symptomatic treatment of Parkinson's disease, but chronic use is associated with L-DOPA-induced dyskinesia in more than half the patients after 10 years of treatment. L-DOPA treatment may affect tryptophan metabolism via the kynurenine pathway. Altered levels of kynurenine metabolites can affect glutamatergic transmission and may play a role in the development of L-DOPA-induced dyskinesia. In this study we assessed kynurenine metabolites in plasma and cerebrospinal fluid of Parkinson's disease patients and controls...
June 19, 2017: Journal of Neurochemistry
https://www.readbyqxmd.com/read/28628197/vesicular-acetylcholine-transporter-vacht-overexpression-induces-major-modifications-of-striatal-cholinergic-interneuron-morphology-and-function
#10
Helena Janickova, Vania F Prado, Marco A M Prado, Salah El Mestikawy, Véronique Bernard
Striatal cholinergic interneurons (CIN) are pivotal for the regulation of the striatal network. Acetylcholine (ACh) released by CIN is centrally involved in reward behavior as well as locomotor or cognitive functions. Recently, BAC transgenic mice expressing channelrhodopsin-2 (ChR2) protein under the control of the choline acetyltransferase (ChAT) promoter (ChAT-ChR2) and displaying almost 50 extra copies of the VAChT gene were used to dissect cholinergic circuit connectivity and function using optogenetic approaches...
June 19, 2017: Journal of Neurochemistry
https://www.readbyqxmd.com/read/28628196/molecular-mechanisms-of-experience-dependent-maturation-in-cortical-gabaergic-inhibition
#11
REVIEW
M Ridzwana Begum, Judy C G Sng
Critical periods (CP) in early postnatal life are periods of plasticity during which the neuronal circuitry is most receptive to environmental stimuli. These early experiences translate to a more permanent and sophisticated neuronal connection in the adult brain systems. Multiple studies have pointed to the development of inhibitory circuitry as one of the central factors for the onset of critical periods. We discuss several molecular mechanisms regulating inhibitory circuit maturation and CP, from gene transcription level to protein signaling level...
June 19, 2017: Journal of Neurochemistry
https://www.readbyqxmd.com/read/28608560/endocannabinoid-system-in-neurodegenerative-disorders
#12
REVIEW
Balapal S Basavarajappa, Madhu Shivakumar, Vikram Joshi, Shivakumar Subbanna
Most neurodegenerative disorders (NDDs) are characterized by cognitive impairment and other neurological defects. The definite cause of and pathways underlying the progression of these NDDs are not well defined. Several mechanisms have been proposed to contribute to the development of NDDs. These mechanisms may proceed concurrently or successively, and they differ among cell types at different developmental stages in distinct brain regions. The endocannabinoid system, which involves cannabinoid receptors type 1 (CB1R) and type 2 (CB2R), endogenous cannabinoids and the enzymes that catabolize these compounds, has been shown to contribute to the development of NDDs in several animal models and human studies...
June 13, 2017: Journal of Neurochemistry
https://www.readbyqxmd.com/read/28608535/discovery-and-characterization-of-two-novel-cb1-receptor-splice-variants-with-modified-n-termini-in-mouse
#13
Sabine Ruehle, James Wager-Miller, Alex Straiker, Jill Farnsworth, Michelle N Murphy, Sebastian Loch, Krisztina Monory, Ken Mackie, Beat Lutz
Numerous studies have been carried out in the mouse model, investigating the role of the CB1 cannabinoid receptor. However, mouse CB1 (mCB1) receptor differs from human CB1 (hCB1) receptor in 13 amino acid residues. Two splice variants, hCB1a and hCB1b, diverging in their amino-termini, have been reported to be unique for hCB1 and, via different signaling properties, contribute to CB1 receptor physiology and pathophysiology. We hypothesized that splice variants also exist for the mCB1 receptor and have different signaling properties...
June 13, 2017: Journal of Neurochemistry
https://www.readbyqxmd.com/read/28608461/epidermal-growth-factor-signals-attenuate-phenotypic-and-functional-development-of-neocortical-gaba-neurons
#14
Hisaaki Namba, Tadasato Nagano, Eiichi Jodo, Satoshi Eifuku, Masao Horie, Hirohide Takebayashi, Yuriko Iwakura, Hidekazu Sotoyama, Nobuyuki Takei, Hiroyuki Nawa
Phenotypic development of neocortical GABA neurons is highly plastic and promoted by various neurotrophic factors such as neuregulin-1. A subpopulation of GABA neurons expresses not only neuregulin receptor (ErbB4) but also epidermal growth factor (EGF) receptor (ErbB1) during development, but the neurobiological action of EGF on this cell population is less understood than that of neuregulin-1. Here we examined the effects of exogenous EGF on immature GABA neurons both in culture and in vivo and also explored physiological consequences in adults...
June 13, 2017: Journal of Neurochemistry
https://www.readbyqxmd.com/read/28581641/clk1-regulated-aerobic-glycolysis-is-involved-in-gliomas-chemoresistance
#15
Li Zhang, Huicui Yang, Wenbin Zhang, Zhongqin Liang, Qiang Huang, Guoqiang Xu, Xuechu Zhen, Long Tai Zheng
Chemoresistance remains a major challenge for the treatment of glioma. In the present study, we investigated the role of Clk1, which encodes an enzyme that is necessary for ubiquinone biosynthesis in glioma chemoresistance in vitro. The results showed that Clk1 was highly expressed in GL261 mouse glioma cells which were most sensitive to BCNU while was expressed in BCNU resistant cells such as glioma cancer stem cells: T98G, U87MG and U251 glioma cells at low levels. Knockdown of Clk1 in GL261 glioma cells significantly reduced BCNU- or cisplatin- induced cell apoptosis whereas the proliferative activity and the expression of multi-drug resistance -related genes including MDR1, MGMT and GSTP1 were not changed...
June 5, 2017: Journal of Neurochemistry
https://www.readbyqxmd.com/read/28581635/targeted-unlabeled-mrm-analysis-of-cell-markers-for-the-study-of-sample-heterogeneity-in-isolated-rat-brain-cortical-microvessels
#16
David Gomez-Zepeda, Catarina Chaves, Meryam Taghi, Philippe Sergent, Wang-Qing Liu, Cerina Chhuon, Michel Vidal, Martin Picard, Elizabeth Thioulouse, Isabelle Broutin, Ida-Chiara Guerrera, Jean-Michel Scherrmann, Yannick Parmentier, Xavier Decleves, Marie-Claude Menet
LC-MS/MS-based targeted absolute protein quantification (in fmol of the analyte protein per μg of total protein) is employed for the molecular characterization of the blood brain barrier (BBB) using isolated brain microvessels. Nevertheless, the heterogeneity of the sample regarding the levels of different cells co-isolated within the microvessels and BSA contamination (from buffers) are not always evaluated. We developed an unlabeled targeted LC-MS/MS method to survey the levels of endothelial cells (ECs), astrocytes and pericytes, as well as BSA contaminant in rat cortical microvessels...
June 5, 2017: Journal of Neurochemistry
https://www.readbyqxmd.com/read/28556983/pink1-regulates-mitochondrial-trafficking-in-dendrites-of-cortical-neurons-through-mitochondrial-pka
#17
Tania DasBanerjee, Raul Y Dagda, Marisela Dagda, Charleen T Chu, Monica Rice, Emmanuel Vazquez-Mayorga, Ruben K Dagda
Mitochondrial Protein Kinase A (PKA) and PTEN-induced kinase 1 (PINK1), which is linked to Parkinson's disease, are two neuroprotective serine/threonine kinases that regulate dendrite remodeling, and mitochondrial function. We have previously shown that PINK1 regulates dendrite morphology by enhancing PKA activity. Here, we show the molecular mechanisms by which PINK1 and PKA in the mitochondrion interact to regulate dendrite remodeling, mitochondrial morphology, content, and trafficking in dendrites. PINK1-deficient cortical neurons exhibit impaired mitochondrial trafficking, reduced mitochondrial content, fragmented mitochondria, and a reduction in dendrite outgrowth compared to wild-type neurons...
May 30, 2017: Journal of Neurochemistry
https://www.readbyqxmd.com/read/28555889/reduced-muscle-strength-in-ether-lipid-deficient-mice-is-accompanied-by-altered-development-and-function-of-the-neuromuscular-junction
#18
Fabian Dorninger, Ruth Herbst, Bojana Kravic, Bahar Z Camurdanoglu, Igor Macinkovic, Gerhard Zeitler, Sonja Forss-Petter, Siegfried Strack, Muzamil Majid Khan, Hans R Waterham, Rüdiger Rudolf, Said Hashemolhosseini, Johannes Berger
Inherited deficiency in ether lipids, a subgroup of phospholipids whose biosynthesis needs peroxisomes, causes the fatal human disorder rhizomelic chondrodysplasia punctata. The exact roles of ether lipids in the mammalian organism and, therefore, the molecular mechanisms underlying the disease are still largely enigmatic. Here, we used the glyceronephosphate O-acyltransferase knockout (Gnpat KO) mouse to study the consequences of complete inactivation of ether lipid biosynthesis and documented substantial deficits in motor performance and muscle strength of these mice...
May 29, 2017: Journal of Neurochemistry
https://www.readbyqxmd.com/read/28547865/re-imagining-alzheimer-s-disease-the-diminishing-importance-of-amyloid-and-a-glimpse-of-what-lies-ahead
#19
REVIEW
Kai-Hei Tse, Karl Herrup
Many have criticized the amyloid cascade hypothesis of Alzheimer's disease for its inconsistencies and failures to either accurately predict disease symptoms or guide the development of productive therapies. In addition to criticisms, however, we believe that the field would benefit from having alternative narratives and disease models that can either replace or function alongside of an amyloid-centric view of Alzheimer's. This review is an attempt to meet that need. We offer three experimentally verified amyloid-independent mechanisms, each of which plausibly contributes substantially to the aetiology of Alzheimer's disease: loss of DNA integrity, faulty cell cycle regulation, regression of myelination...
May 26, 2017: Journal of Neurochemistry
https://www.readbyqxmd.com/read/28547849/heparan-sulfate-alterations-in-extracellular-matrix-structures-and-fgf-2-signaling-impairment-in-the-aged-neurogenic-niche
#20
Taihei Yamada, Aurelien Kerever, Yusuke Yoshimura, Yuji Suzuki, Risa Nonaka, Kyohei Higashi, Toshihiko Toida, Frederic Mercier, Eri Arikawa-Hirasawa
Adult neurogenesis in the subventricular zone of the lateral ventricle decreases with age. In the subventricular zone, the specialized extracellular matrix structures, known as fractones, contact neural stem cells and regulate neurogenesis. Fractones are composed of extracellular matrix components, such as heparan sulfate proteoglycans. We previously found that fractones capture and store fibroblast growth factor 2 (FGF-2) via heparan sulfate binding, and may deliver FGF-2 to neural stem cells in a timely manner...
May 26, 2017: Journal of Neurochemistry
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