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Journal of Neurochemistry

Anne I Boullerne, Joyce A Benjamins, Alex Chiu, Naren L Banik
No abstract text is available yet for this article.
December 13, 2018: Journal of Neurochemistry
Yeming Yang, Wenjing Liu, Kuanxiang Sun, Li Jiang, Xianjun Zhu
Phospholipids are asymmetrically distributed across the mammalian plasma membrane, with phosphatidylserine (PS) and phosphatidylethanolamine (PE) concentrated in the cytoplasmic leaflet of the membrane bilayer and phosphatidylcholine in the exoplasmic leaflet. This asymmetric distribution is dependent on a group of P4 ATPases called PS flippases. The proper transport and function of PS flippases require a β-subunit transmembrane protein 30A (TMEM30A). Disruption of PS flippases leads to several human diseases...
December 12, 2018: Journal of Neurochemistry
Neil T Sprenkle, Anirudhya Lahiri, James W Simpkins, Gordon P Meares
Improper protein folding and trafficking are common pathological events in neurodegenerative diseases that result in the toxic accumulation of misfolded proteins within the lumen of the endoplasmic reticulum (ER). While low-level stimulation of the unfolded protein response (UPR) is protective, sustained UPR activation resulting from prolonged ER stress can promote neurotoxicity. The cell-autonomous mechanisms of the UPR have been extensively characterized. However, the cell-extrinsic role of the UPR under physiological and pathological states in the central nervous system (CNS) remains to be elucidated...
December 6, 2018: Journal of Neurochemistry
Xinwen Zhang, Matthew V Green, Stanley A Thayer
HIV-associated neurocognitive disorder (HAND) affects about half of HIV-infected patients. HIV impairs neuronal function through indirect mechanisms mainly mediated by inflammatory cytokines and neurotoxic viral proteins, such as the envelope protein gp120. HIV gp120 elicits a neuroinflammatory response that potentiates NMDA receptor function and induces the loss of excitatory synapses. How gp120 influences neuronal inhibition is not known. In this study, we expressed a green fluorescent protein (GFP)-tagged recombinant antibody-like protein that binds to the post-synaptic scaffolding protein gephyrin to label inhibitory synapses in living neurons...
December 6, 2018: Journal of Neurochemistry
Ke Xu, Yong He, Xi Chen, Yu Tian, Ke Cheng, Lu Zhang, Yue Wang, Deyu Yang, Haiyang Wang, Zhonghao Wu, Yan Li, Tianlan Lan, Zhifang Dong, Peng Xie
The proportion of major depressive disorder (MDD) patients around the world has increased remarkably. Although many studies of MDD have been conducted based on classic hypotheses, like alteration of the hypothalamic-pituitary-adrenal axis or monoamine neurotransmitters, the mechanisms underlying MDD remain unclear. Aiming to further investigate the mechanisms of MDD, liquid-chromatography tandem mass spectrometry was employed to measure target metabolites in the hippocampus (HIPPO) of chronic social defeat stress (CSDS) model mice...
December 6, 2018: Journal of Neurochemistry
Berzenn Urbi, Maame Amma Owusu, Ian Hughes, Matthew Katz, Simon Broadley, Arman Sabet
Amyotrophic Lateral Sclerosis (ALS) is a neurodegenerative disorder that results from motor neuron damage. Cannabinoids have been proposed as treatments for ALS due to their anti-excitotoxicity, anti-oxidant, and anti-inflammatory effects. Pre-clinical studies in mice models of ALS have been published using a range of cannabinoid formulations and doses. To date, there has been no rigorous evaluation of these trials to assess a potential cannabinoid treatment effect. This review and meta-analysis was undertaken to provide evidence for or against a treatment effect of cannabinoids in murine ALS models...
December 6, 2018: Journal of Neurochemistry
Mahmoud Yousefifard, Arash Sarveazad, Asrin Babahajian, Masoud Baikpour, Farhad Shokraneh, Alexander R Vaccaro, James S Harrop, Michael G Fehlings, Mostafa Hosseini, Vafa Rahimi-Movaghar
It remains unclear whether biomarkers in the serum or cerebrospinal fluid (CSF) can be used for diagnosis or prognosis of spinal cord injuries (SCI). Therefore, a systematic review was undertaken to evaluate the prognostic or diagnostic value of serum and CSF biomarkers in assessing the severity of SCI and the outcome of patients. Two independent reviewers summarized the human studies retrieved from the electronic databases of Medline, Embase, Scopus and ISI Web of Science until April 2018. Seventeen studies were included (1065 patients aged 16 to 94 years old)...
November 29, 2018: Journal of Neurochemistry
Hye Guk Ryu, Sangjune Kim, Saebom Lee, Eunju Lee, Hyo-Jin Kim, Do-Yeon Kim, Kyong-Tai Kim
Misfolded proteins with abnormal polyglutamine (polyQ) expansion cause neurodegenerative disorders, including Huntington's disease (HD). Recently, it was found that polyQ aggregates accumulate due to vaccinia-related kinase 2 (VRK2)-mediated degradation of TCP-1 ring complex (TRiC)/Chaperonin-containing TCP-1 (CCT), which has an essential role in the prevention of polyQ protein aggregation and cytotoxicity. The levels of VRK2 are known to be much higher in actively proliferating cells but are maintained at a low level in the brain via an unknown mechanism...
November 29, 2018: Journal of Neurochemistry
Na Yu, Xin Wang, Haibo Bao, Zewen Liu
Insect nicotinic acetylcholine receptors (nAChRs) are not only important neuro-transmitter receptors but also effective insecticide targets. The regulation of nAChRs has been mainly studied in vertebrates especially in mammals. Here, two types of nAChRs were found present in the locust Locusta migratoria mamilensis dorsal unpaired median (DUM) neurons, α-bungarotoxin (α-Bgt)-sensitive nAChRs and α-Bgt-resistant nAChRs, responding to acetylcholine (ACh) at different concentrations. The homologues to three mammalian nAChR regulators, ubiquilin-1, CRELD2 (Cysteine-rich with EFG-like domain 2) and PICK1 (protein interacting with PRKCA 1), were characterised in L...
November 28, 2018: Journal of Neurochemistry
Eugene M Cilento, Lorrain Jin, Tessandra Stewart, Min Shi, Lifu Sheng, Jing Zhang
Accurate, reliable, and objective biomarkers for Alzheimer's disease (AD), Parkinson's disease (PD), and related age-associated neurodegenerative disorders are urgently needed to assist in both diagnosis, particularly at early stages, and monitoring of disease progression. Technological advancements in protein detection platforms over the last few decades have resulted in a plethora of reported molecular biomarker candidates for both AD and PD; however, very few of these candidates are developed beyond the discovery phase of the biomarker discovery pipeline, a reflection of the current bottleneck within the field...
November 26, 2018: Journal of Neurochemistry
Wenzhang Wang, Xiongwei Zhu
ε4 allele of ApoE is the strongest genetic risk factor for late onset Alzheimer's disease (AD). Supplementation of ApoE proteins or mimetics has been pursued for drug developments against AD. A very low-density lipoprotein (HDL) mimetic peptide 4F was shown to alleviate AD-related deficits in APP transgenic mice, and this editorial highlights a study by Chernick et al. who use both mouse and human neuroglial cells to explore the mechanism underlying beneficial effects of this peptide. The authors demonstrate that 4F peptide significantly increased the secretion and lipidation of ApoE in the absence and presence of Aβ independent of de novo transcription/translation, but requiring ABCA1 and the integrity of the secretory pathway between ER and Golgi...
November 26, 2018: Journal of Neurochemistry
Bert J C Janssen
Our nervous system depends on protein-mediated cellular communication and connections for its formation and function. The transmembrane receptor Myelin-Associated Glycoprotein (MAG) plays an important role in the wrapping process of myelin around axons and in life-long maintenance of this important bicellular structure. MAG organizes the adhesion and the signalling between the axon and the myelin. But how does MAG do this? Better understanding of this process is required to treat MAG-function associated neurological disorders...
November 26, 2018: Journal of Neurochemistry
Erin R Hascup, Sarah O Broderick, Mary K Russell, Yimin Fang, Andrzej Bartke, Heather A Boger, Kevin N Hascup
The symptomologies of Alzheimer's disease (AD) develop over decades suggesting modifiable life-style factors may contribute to disease pathogenesis. In humans, hyperinsulinemia associated with type 2 diabetes mellitus increases the risk for developing AD and both diseases share similar age-related etiologies including amyloidogenesis. Since we have demonstrated that soluble Aβ42 elicits glutamate release, we wanted to understand how diet-induced insulin resistance alters hippocampal glutamate dynamics, which are important for memory formation and consolidation...
November 25, 2018: Journal of Neurochemistry
Tristan R Hollyer, Luca Bordoni, Birgitte S Kousholt, Judith van Luijk, Merel Ritskes-Hoitinga, Leif Østergaard
Lactate's role in the brain is understood as a contributor to brain energy metabolism, but it may also regulate the cerebral microcirculation. The purpose of this systematic review is to evaluate evidence of lactate as a physiological effector within the normal cerebral microcirculation in reports ranging from in vitro experiments to in vivo studies in animals and humans. Following pre-registration of a review protocol, we systematically searched the PubMed, EMBASE, and Cochrane databases for literature covering themes of 'lactate', 'the brain', and 'microcirculation'...
November 25, 2018: Journal of Neurochemistry
Helen Parker, Brian W Bigger
Mucopolysaccharidoses are lysosomal storage disorders characterised by accumulation of abnormal pathological glycosaminoglycans, cellular dysfunction and widespread inflammation, resulting in progressive cognitive and motor decline. Lysosomes are important mediators of immune cell function, and therefore accumulation of GAGs and other abnormal substrates could affect immune function and directly impact on disease pathogenesis. This review summarises current knowledge with regards to inflammation in mucopolysaccharidosis with an emphasis on the brain and outlines a potential role for GAGs in induction of inflammation...
November 19, 2018: Journal of Neurochemistry
Jada H Vaden, Tina Tian, Samantha Golf, John W McLean, Julie A Wilson, Scott M Wilson
Ubiquitin is an essential signaling protein that controls many different cellular processes. While cellular ubiquitin levels normally cycle between pools of free and conjugated ubiquitin, the balance of these ubiquitin pools can be shifted by exposure to a variety of cellular stresses. Altered ubiquitin pools are also observed in several neurological disorders, suggesting that imbalances in ubiquitin homeostasis may contribute to neuronal dysfunction. To examine the effects of increased ubiquitin levels on the mammalian nervous system, we generated transgenic mice that express ubiquitin under the control of the Thy1...
November 19, 2018: Journal of Neurochemistry
Meisam Rostaminasab Dolatabad, Lu-Lu Guo, Peng Xiao, Zhongliang Zhu, Qing-Tao He, Du-Xiao Yang, Chang-Xiu Qu, Sheng-Chao Guo, Xiao-Lei Fu, Rui-Rui Li, Lin Ge, Ke-Jia Hu, Liu Hong-da, Yue-Mao Shen, Xiao Yu, Jin-Peng Sun, Peng-Ju Zhang
Protein Phosphatase Mg2+ /Mn2+ Dependent 1K (PPM1K),also named as PP2Cm or branched-chain α-ketoacid dehydrogenase complex phosphatase (BDP), is a member of the metal-dependent phosphatase family and an important metabolic regulator. Single nucleotide polymorphisms (SNPs) in PPM1K contributing to protein functional defects have been found to be associated with numerous human diseases, such as cardiovascular disease, maple syrup urine disease, type 2 diabetes, and neurological disease. PPM1K N94K is an identified missense mutant produced by one of the SNPs in the human PPM1K coding sequence...
November 19, 2018: Journal of Neurochemistry
K Genevieve Feldmann, Ayesha Chowdhury, Jessi Becker, N'Gina McAlpin, Taqwa Ahmed, Syed Haider, Jian X Richard Xia, Karina Diaz, Monal G Mehta, Itzhak Mano
Excitotoxicity, caused by exaggerated neuronal stimulation by Glutamate (Glu), is a major cause of neurodegeneration in brain ischemia. While we know that neurodegeneration is triggered by overstimulation of Glu-Receptors (GluRs), the subsequent mechanisms that lead to cellular demise remain controversial. Surprisingly, signaling downstream of GluRs can also activate neuroprotective pathways. The strongest evidence involves activation of the transcription factor cAMP Response Element Binding-protein (CREB), widely recognized for its importance in synaptic plasticity...
November 16, 2018: Journal of Neurochemistry
Meichun Deng, Shao-Rui Chen, Hong Chen, Yi Luo, Yingchun Dong, Hui-Lin Pan
Opioid-induced hyperalgesia and analgesic tolerance can lead to dose escalation and inadequate pain treatment with μ-opioid receptor agonists. Opioids cause tonic activation of glutamate NMDA receptors (NMDARs) at primary afferent terminals, increasing nociceptive input. However, the signaling mechanisms responsible for opioid-induced activation of pre-synaptic NMDARs in the spinal dorsal horn remain unclear. In this study, we determined the role of MAPK signaling in opioid-induced pre-synaptic NMDAR activation caused by chronic morphine administration...
November 16, 2018: Journal of Neurochemistry
Youfang Chen, Shao-Rui Chen, Hong Chen, Jixiang Zhang, Hui-Lin Pan
Painful peripheral neuropathy is a severe and difficult-to-treat neurological complication associated with cancer chemotherapy. Although chemotherapeutic drugs such as paclitaxel are known to cause tonic activation of presynaptic NMDA receptors (NMDARs) to potentiate nociceptive input, the molecular mechanism involved in this effect is unclear. α2δ-1, commonly known as a voltage-activated calcium channel subunit, is a newly discovered NMDAR-interacting protein and plays a critical role in NMDAR-mediated synaptic plasticity...
November 15, 2018: Journal of Neurochemistry
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