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The role of E3 ubiquitin ligases in synapse function in the healthy and diseased brain Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2021-02-11 Hiroshi Kawabe; Judith Stegmüller
Ubiquitination is a key posttranslational modification for the controlled protein degradation and proteostasis. The substrate specificity is determined by a family of E3 ubiquitin ligases, which are encoded by more than 600 genes in the mammalian genome. Gain- or loss-of-function of a number of E3 genes results in neurodegeneration or neurodevelopmental disorders, affecting synapse function. This implies
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Behavioral profiling reveals an enhancement of dentate gyrus paired pulse inhibition in a rat model of PTSD Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2021-02-03 Anne Albrecht; Elhanan Ben-Yishay; Gal Richter-Levin
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CHRNA1 promotes the pathogenesis of primary focal hyperhidrosis Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2021-01-19 Jian-Bo Lin; Ming-Qiang Kang; Li-Ping Huang; Yi Zhuo; Xu Li; Fan-Cai Lai
The aim of the study was to elucidate the involvement of cholinergic receptor nicotinic alpha 1 subunit (CHRNA1) in the pathogenesis of primary focal hyperhidrosis (PFH). The hyperhidrosis mouse model was constructed using pilocarpine injection. The expression levels of CHRNA1 in sweat gland tissues of PFH patients and hyperhidrosis mice were compared using Western blots and quantitative real-time
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DNA repair pathways are altered in neural cell models of frataxin deficiency Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2021-01-06 Jara Moreno-Lorite; Sara Pérez-Luz; Yurika Katsu-Jiménez; Daniel Oberdoerfer; Javier Díaz-Nido
Friedreich's ataxia (FRDA) is a hereditary and predominantly neurodegenerative disease caused by a deficiency of the protein frataxin (FXN). As part of the overall efforts to understand the molecular basis of neurodegeneration in FRDA, a new human neural cell line with doxycycline-induced FXN knockdown was established. This cell line, hereafter referred to as iFKD-SY, is derived from the human neuroblastoma
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Macrophage roles in peripheral nervous system injury and pathology: Allies in neuromuscular junction recovery Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2021-01-08 Rachel Rios; Albina Jablonka-Shariff; Curtis Broberg; Alison K. Snyder-Warwick
Peripheral nerve injuries remain challenging to treat despite extensive research on reparative processes at the injury site. Recent studies have emphasized the importance of immune cells, particularly macrophages, in recovery from nerve injury. Macrophage plasticity enables numerous functions at the injury site. At early time points, macrophages perform inflammatory functions, but at later time points
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Endogenous Aβ peptide promote Aβ oligomerization tendency of spiked synthetic Aβ in Alzheimer's disease plasma Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2021-01-08 Youngki Choi; Yechan Joh; Ji Sun Ryu; Kaylen Kim; David Seo; SangYun Kim
Alzheimer's disease (AD) is the most common form of age-associated dementia. Several studies have predicted that AD is caused by the production and deposition of the β-amyloid peptide (Aβ) in the brain, which is one of pathologic hallmarks of AD. In particular, Aβ oligomers are reportedly the most toxic and pathogenic of other peptide forms. We previously developed Multimer Detection System-Oligomeric
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Hepcidin inhibits autophagy in intracerebral hemorrhage models in vitro and in vivo Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2021-01-08 Chao Zhang; Christopher Qian; Guang Yang; Yu-Xin Bao; Zhong-Ming Qian
Iron has a key role in the activation of the autophagic pathway in rats with intracerebral hemorrhage (ICH), and hepcidin has the ability to reduce brain iron in ICH-rats. We therefore hypothesized that hepcidin might be able to inhibit autophagy by reducing iron in an ICH brain. Here, we investigated the effects of Ad-hepcidin and/or hepcidin peptide on autophagic activities in ICH models in vitro
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Unexpected role of stress as a possible resilience mechanism upon mild traumatic brain injury (mTBI) in mice Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2021-01-04 Efrat Shavit-Stein; Alexandra Gerasimov; Shay Aharoni; Shany G. Gofrit; Ellen Pikus; Chaim G. Pick; Nicola Maggio
Introduction Mild traumatic brain injury (mTBI) is common and associated with cognitive impairment. Stress and mTBI are known to modulate the neural function. The present study aims at exploring the effect of prior stress exposure on cognitive function following mTBI. Methods Eight weeks old male ICR mice were subjected to either stress induced by forced swimming stress alone, stress followed by an
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Inhibitory signaling in mammalian olfactory transduction potentially mediated by Gαo Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-12-25 Elizabeth A. Corey; Kirill Ukhanov; Yuriy V. Bobkov; Jeremy C. McIntyre; Jeffrey R. Martens; Barry W. Ache
Olfactory GPCRs (ORs) in mammalian olfactory receptor neurons (ORNs) mediate excitation through the Gαs family member Gαolf. Here we tentatively associate a second G protein, Gαo, with inhibitory signaling in mammalian olfactory transduction by first showing that odor evoked phosphoinositide 3-kinase (PI3K)-dependent inhibition of signal transduction is absent in the native ORNs of mice carrying a
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Resilience to fear: The role of individual factors in amygdala response to stressors Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-12-18 Rosalina Fonseca; Natália Madeira; Carla Simoes
Resilience to stress is an adaptive process that varies individually. Resilience refers to the adaptation, or the ability to maintain or regain mental health, despite being subject to adverse situation. Resilience is a dynamic concept that reflects a combination of internal individual factors, including age and gender interacting with external factors such as social, cultural and environmental factors
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Neuroprotection with the cannabigerol quinone derivative VCE-003.2 and its analogs CBGA-Q and CBGA-Q-Salt in Parkinson's disease using 6-hydroxydopamine-lesioned mice Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-12-16 Sonia Burgaz; Concepción García; María Gómez-Cañas; Carmen Navarrete; Adela García-Martín; Alain Rolland; Carmen del Río; María J. Casarejos; Eva Muñoz; Claudia Gonzalo-Consuegra; Eduardo Muñoz; Javier Fernández-Ruiz
The quinone derivative of the non-psychotropic cannabinoid cannabigerol (CBG), so-called VCE-003.2, has been recently investigated for its neuroprotective properties in inflammatory models of Parkinson's disease (PD) in mice. Such potential derives from its activity at the peroxisome proliferator-activated receptor-γ (PPAR-γ). In the present study, we investigated the neuroprotective properties of
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Blockade of metabotropic glutamate receptor 5 attenuates axonal degeneration in 6-hydroxydopamine-induced model of Parkinson's disease Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-11-25 Jian-Nan Zhang; Yan-Lin Huang; Hui-Min Yang; Yuan Wang; Li Gu; Hong Zhang
Although there are numerous strategies to counteract the death of dopaminergic neurons in Parkinson's disease (PD), there are currently no treatments that delay or prevent the disease course, indicating that early protective treatments are needed. Targeting axonal degeneration, a key initiating event in PD, is required to develop novel therapies; however, its underlying molecular mechanisms are not
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Polyglutamine expanded Ataxin-7 induces DNA damage and alters FUS localization and function Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-12-16 Frida Niss; Wajiha Zaidi; Einar Hallberg; Anna-Lena Ström
Polyglutamine (polyQ) diseases, such as Spinocerebellar ataxia type 7 (SCA7), are caused by expansions of polyQ repeats in disease specific proteins. The sequestration of vital proteins into aggregates formed by polyQ proteins is believed to be a common pathological mechanism in these disorders. The RNA-binding protein FUS has been observed in polyQ aggregates, though if disruption of this protein
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In vitro priming response in dorsal root ganglia partially mimics injury-driven pre-conditioning response and reprograms neurons for enhanced outgrowth Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-11-25 Anand Krishnan; Shubham Dwivedi; Ambika Chandrasekhar; Aparna Areti; Douglas W. Zochodne
Peripheral nerve injuries have the potential to bring about long-term disabilities in individuals. The major issue in repairing nerve injuries is the poor growth rate of axons. Although several molecules have been identified as potential candidates for improving axon growth, their potential translation into clinical practice is preliminary and largely unexplored. This necessitates identifying additional
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The dietary fatty acids α-linolenic acid (ALA) and linoleic acid (LA) selectively inhibit microglial nitric oxide production Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-11-06 Jessica R. Lowry; Nick Marshall; Tyler J. Wenzel; Taryn E. Murray; Andis Klegeris
Alzheimer's disease (AD) is a neurodegenerative disorder without a known cure or effective treatment. Research has identified several modifiable risk factors and suggested preventative measures to reduce the risk of developing AD, including alterations in diet. Polyunsaturated fatty acids (PUFAs) have been shown to regulate inflammatory responses in the central nervous system (CNS), the main site of
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When glia meet induced pluripotent stem cells (iPSCs) Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-10-14 Li Li; Yanhong Shi
The importance of glial cells, mainly astrocytes, oligodendrocytes, and microglia, in the central nervous system (CNS) has been increasingly appreciated. Recent advances have demonstrated the diversity of glial cells and their contribution to human CNS development, normal CNS functions, and disease progression. The uniqueness of human glial cells is also supported by multiple lines of evidence. With
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Tip60 protects against amyloid-β-induced transcriptomic alterations via different modes of action in early versus late stages of neurodegeneration Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-11-04 Haolin Zhang; Bhanu Chandra Karisetty; Akanksha Bhatnagar; Ellen M. Armour; Mariah Beaver; Tiffany V. Roach; Sina Mortazavi; Shreya Mandloi; Felice Elefant
Alzheimer's disease (AD) is an age-related neurodegenerative disorder hallmarked by amyloid-β (Aβ) plaque accumulation, neuronal cell death, and cognitive deficits that worsen during disease progression. Histone acetylation dysregulation, caused by an imbalance between reduced histone acetyltransferases (HAT) Tip60 and increased histone deacetylase 2 (HDAC2) levels, can directly contribute to AD pathology
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Regulation of actin dynamics in dendritic spines: Nanostructure, molecular mobility, and signaling mechanisms Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-10-20 Shigeo Okabe
Dendritic spines are major sites of excitatory synaptic connection in pyramidal neurons of the forebrain, and their functional regulation underlies the development of functional neuronal circuits and experience-dependent circuit plasticity. Dendritic spines contain a large amount of actin filaments, and their organization and dynamics control both the morphology and function of dendritic spines. New
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Enduring neuroimmunological consequences of developmental experiences: From vulnerability to resilience Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-10-14 Jack Reddaway; Nichola M. Brydges
The immune system is crucial for normal neuronal development and function (neuroimmune system). Both immune and neuronal systems undergo significant postnatal development and are sensitive to developmental programming by environmental experiences. Negative experiences from infection to psychological stress at a range of different time points (in utero to adolescence) can permanently alter the function
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Postganglionic sympathetic neurons, but not locus coeruleus optostimulation, activates neuromuscular transmission in the adult mouse in vivo Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-10-08 Zhong-Min Wang; Maria L. Messi; Valentina Grinevich; Evgeny Budygin; Osvaldo Delbono
Recent work demonstrated that sympathetic neurons innervate the skeletal muscle near the neuromuscular junction (NMJ), and muscle sympathectomy and sympathomimetic agents strongly influence motoneuron synaptic vesicle release ex vivo. Moreover, reports attest that the pontine nucleus locus coeruleus (LC) projects to preganglionic sympathetic neurons and regulates human mobility and skeletal muscle
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Cannabinoid receptor subtype influence on neuritogenesis in human SH-SY5Y cells Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-10-10 Erica L. Lyons; Sandra Leone-Kabler; Alexander L. Kovach; Brian F. Thomas; Allyn C. Howlett
Human SH-SY5Y neuroblastoma cells stably expressing exogenous CB1 (CB1XS) or CB2 (CB2XS) receptors were developed to investigate endocannabinoid signaling in the extension of neuronal projections. Expression of cannabinoid receptors did not alter proliferation rate, viability, or apoptosis relative to parental SH-SY5Y. Transcripts for endogenous cannabinoid system enzymes (diacylglycerol lipase, monoacylglycerol
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Molecular correlates of mitochondrial dysfunctions in major depression: Evidence from clinical and rodent studies Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-09-23 Virginie Rappeneau; Lars Wilmes; Chadi Touma
Major depressive disorder (MDD) is one of the most prevalent stress-related mental disorders worldwide. Several biological mechanisms underlying the pathophysiology of MDD have been proposed, including endocrine disturbances, neurotransmitter deficits, impaired neuronal plasticity, and more recently, mitochondrial dysfunctions. In this review, we provide an overview of relevant molecular correlates
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Dissecting Alzheimer’s disease pathogenesis in human 2D and 3D models Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-10-14 Giovanna Cenini; Matthias Hebisch; Vira Iefremova; Lea J. Flitsch; Yannik Breitkreuz; Rudolph E. Tanzi; Doo Yeon Kim; Michael Peitz; Oliver Brüstle
The incidence of Alzheimer’s disease (AD) is increasing with the aging population, and it has become one of the main health concerns of modern society. The dissection of the underlying pathogenic mechanisms and the development of effective therapies remain extremely challenging, also because available animal and cell culture models do not fully recapitulate the whole spectrum of pathological changes
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Modelling Frontotemporal Dementia using patient-derived induced pluripotent stem cells. Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-09-19 Georgie Lines,Jackie M Casey,Elisavet Preza,Selina Wray
Frontotemporal dementia (FTD) describes a group of clinically heterogeneous conditions that frequently affect people under the age of 65 (Le Ber et al., 2013). There are multiple genetic causes of FTD, including coding or splice-site mutations in MAPT, GRN mutations that lead to haploinsufficiency of progranulin protein, and a hexanucleotide GGGGCC repeat expansion in C9ORF72. Pathologically, FTD is
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Erythropoietin modulates striatal antioxidant signalling to reduce neurodegeneration in a toxicant model of Parkinson's disease Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-09-21 A.M. Thompson; K. Farmer; E.M. Rowe; S. Hayley
The current study sought to characterize the pro-survival effects of erythropoietin (EPO) in a toxicant model of Parkinson's disease (PD). EPO treatment induced time-dependent elevations of antioxidant glutathione peroxidase (GPx) and anti-apoptotic factors (pAkt and pBad/Bad) within the striatum and substantia nigra pars compacta (SNc). Intriguingly, our results indicated a region- and lesion size-
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Characterization hiPSC-derived neural progenitor cells and neurons to investigate the role of NOS1AP isoforms in human neuron dendritogenesis Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-09-26 Christen M. Crosta; Kristina Hernandez; Atul K. Bhattiprolu; Allen Y. Fu; Jennifer C. Moore; Stephen G. Clarke; Natasha R. Dudzinski; Linda M. Brzustowicz; Kenneth G. Paradiso; Bonnie L. Firestein
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Matrix metalloprotease-mediated cleavage of neural glial-related cell adhesion molecules activates quiescent olfactory stem cells via EGFR. Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-09-18 Zhen-Huang Chen,Xiao-Cui Luo,C Ron Yu,Liquan Huang
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Sympathomimetics regulate quantal acetylcholine release at neuromuscular junctions through various types of adrenoreceptors. Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-09-02 Andrei Tsentsevitsky,Leniz Nurullin,Oksana Tyapkina,Ellya Bukharaeva
The studies of the interaction between the sympathetic and motor nervous systems are extremely relevant due to therapy for many neurodegenerative and cardiovascular disorders involving adrenergic compounds. Evidences indicate close contact between sympathetic varicosities and neuromuscular synapses. This raises questions about the effects of catecholamines on synaptic transmission. The currently available
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Dystrophic Dmdmdx rats show early neuronal changes (increased S100β and Tau5) at 8 months, supporting severe dystropathology in this rodent model of Duchenne muscular dystrophy. Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-09-02 Vidya S Krishnan,Lakshana P Thanigaiarasu,Robert White,Rachael Crew,Thibaut Larcher,Caroline Le Guiner,Miranda D Grounds
The intrinsic necrosis of skeletal muscles in animal models of Duchenne muscular dystrophy (DMD) damages neuromuscular junctions (NMJs) with progressively altered NMJs associated with denervation and premature changes in dystrophic nerves. In the mdx mouse model of DMD, the proteins S100β and Tau5 are significantly increased in sciatic nerves by 13 months (M) of age, far earlier (by 9 M) than in normal
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P38K and JNK pathways are induced by amyloid-β in astrocyte: Implication of MAPK pathways in astrogliosis in Alzheimer's disease. Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-09-05 Pampa Saha,Subhalakshmi Guha,Subhas Chandra Biswas
Astrocyte activation is one of the crucial hallmarks of Alzheimer's disease (AD) along with amyloid-β (Aβ) plaques, neurofibrillary tangles and neuron death. Glial scar and factors secreted from activated astrocytes have important contribution on neuronal health in AD. In this study, we investigated the mechanisms of astrocyte activation both in in vitro and in vivo models of AD. In this regard, mitogen
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Effects of RU486 treatment after single prolonged stress depend on the post-stress interval. Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-08-25 Jinlan Ding,Xinzhao Chen,Marcia Santos da Silva,Jolanthe Lingeman,Fang Han,Onno C Meijer
The Single Prolonged Stress protocol is considered a model for PTSD, as it induces long lasting changes in rat behaviour and endocrine regulation. Previous work demonstrated that some of these changes can be prevented by treatment with the glucocorticoid receptor antagonist RU486, administered a week after the stressor. The current study evaluated the effects of an earlier intervention with RU486,
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Mitochondrial damage-associated molecular patterns stimulate reactive oxygen species production in human microglia. Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-08-20 Milena Nasi,Anna De Gaetano,Elena Bianchini,Sara De Biasi,Lara Gibellini,Anita Neroni,Marco Mattioli,Marcello Pinti,Domenico Lo Tartaro,Rebecca Borella,Anna Vittoria Mattioli,Johanna Chester,Alessandra Melegari,Anna Maria Simone,Diana Ferraro,Francesca Vitetta,Patrizia Sola,Andrea Cossarizza
Microglia are the resident innate immune cells of the central nervous system and exert functions of host defence and maintenance of normal tissue homeostasis, along with support of neuronal processes in the healthy brain. Chronic and dysregulated microglial cell activation has increasingly been linked to the status of neuroinflammation underlying many neurodegenerative diseases, including multiple
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The ubiquitin ligase UBE4B regulates amyloid precursor protein ubiquitination, endosomal trafficking, and amyloid β42 generation and secretion. Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-08-22 Monica Gireud-Goss,Sahily Reyes,Ritika Tewari,Anthony Patrizz,Matthew D Howe,Julia Kofler,M Neal Waxham,Louise D McCullough,Andrew J Bean
The extracellular accumulation of amyloid β (Aβ) fragments of amyloid precursor protein (APP) in brain parenchyma is a pathological hallmark of Alzheimer’s disease (AD). APP can be cleaved into Aβ on late endosomes/multivesicular bodies (MVBs). E3 ubiquitin ligases have been linked to Aβ production, but specific E3 ligases associated with APP ubiquitination that may affect targeting of APP to endosomes
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Norepinephrine and glucocorticoid effects on the brain mechanisms underlying memory accuracy and generalization. Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-08-14 Sevgi Bahtiyar,Kubra Gulmez Karaca,Marloes J A G Henckens,Benno Roozendaal
Stressful and emotionally arousing experiences activate hormonal and brain systems that create strong memories. Extensive evidence indicates that this strengthening effect involves the synergistic action of both norepinephrine and glucocorticoid hormones. This tight regulation of emotional memories is normally highly adaptive and pivotal for survival; yet, aberrant memory processing of stressful events
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Role of induced pluripotent stem cells in lysosomal storage diseases. Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-08-21 Jun Kido,Kimitoshi Nakamura,Takumi Era
Lysosomal storage diseases (LSDs) are a group of metabolism inborn errors caused by defective enzymes in the lysosome, resulting in the accumulation of undegraded substrates. Many characteristic cell features have been revealed in LSDs, including abnormal autophagy and mitochondrial dysfunction. The development of induced pluripotent stem cells (iPSCs) dramatically boosted research on LSDs, particularly
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Application of induced pluripotent stem cells in epilepsy. Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-08-04 Shinichi Hirose,Yasuyoshi Tanaka,Mami Shibata,Yuichi Kimura,Mitsuru Ishikawa,Norimichi Higurashi,Toshiyuki Yamamoto,Eisuke Ichise,Tomohiro Chiyonobu,Atsushi Ishii
Epilepsy is among the most common neurological disorders, affecting approximately 50 million people worldwide. Importantly, epilepsy is genetically and etiologically heterogenous, but several epilepsy types exhibit similar clinical presentations. Epilepsy-associated genes are being identified. However, the molecular pathomechanisms remain largely unknown. Approximately one-third of epilepsy is refractory
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ALS-associated TBK1 variant p.G175S is defective in phosphorylation of p62 and impacts TBK1-mediated signalling and TDP-43 autophagic degradation. Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-08-21 A D Foster,P Downing,E Figredo,N Polain,A Stott,R Layfield,S L Rea
Mutations affecting SQSTM1 coding for p62 and TANK-Binding Kinase 1 (TBK1) have been implicated in amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD). TBK1 is a serine-threonine kinase that regulates p62's activity as an autophagy receptor via phosphorylation and also has roles in neuroinflammatory signalling pathways. The mechanisms underlying ALS and FTLD pathogenesis
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Aging lowers PEX5 levels in cortical neurons in male and female mouse brains. Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-08-07 Ndidi-Ese Uzor,Diego Morales Scheihing,Gab Seok Kim,Jose Felix Moruno-Manchon,Liang Zhu,Caroline R Reynolds,Jessica M Stephenson,Aleah Holmes,Louise D McCullough,Andrey S Tsvetkov
Peroxisomes exist in nearly every cell, oxidizing fats, synthesizing lipids and maintaining redox balance. As the brain ages, multiple pathways are negatively affected, but it is currently unknown if peroxisomal proteins are affected by aging in the brain. While recent studies have investigated a PEX5 homolog in aging C. elegans models and found that it is reduced in aging, it is unclear if PEX5, a
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The effect of axotomy on firing and ultrastructure of the crayfish mechanoreceptor neurons and satellite glial cells. Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-07-24 M V Rudkovskii,A G Fedorenko,A M Khaitin,M A Pitinova,A B Uzdensky
Neurotrauma is among main causes of human disability and death. We studied effects of axotomy on ultrastructure and neuronal activity of a simple model object – an isolated crayfish stretch receptor that consists of single mechanoreceptor neurons (MRN) enwrapped by multilayer glial envelope. After isolation, MRN regularly fired until spontaneous activity cessation. Axotomy did not change significantly
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Models of the blood-brain barrier using iPSC-derived cells. Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-07-24 Louise Delsing,Anna Herland,Anna Falk,Ryan Hicks,Jane Synnergren,Henrik Zetterberg
The blood-brain barrier (BBB) constitutes the interface between the blood and the brain tissue. Its primary function is to maintain the tightly controlled microenvironment of the brain. Models of the BBB are useful for studying the development and maintenance of the BBB as well as diseases affecting it. Furthermore, BBB models are important tools in drug development and support the evaluation of the
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Ih, GIRK, and KCNQ/Kv7 channels differently modulate sharp wave - ripples in the dorsal and ventral hippocampus. Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-07-22 George Trompoukis,Pavlos Rigas,Leonidas J Leontiadis,Costas Papatheodoropoulos
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Integration of CRISPR-engineering and hiPSC-based models of psychiatric genomics. Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-07-23 Marliette R Matos,Seok-Man Ho,Nadine Schrode,Kristen J Brennand
Neuropsychiatric disorders are highly heritable polygenic disorders arising from the complex interplay of highly penetrant rare variants and common variants of small effect. There is a large index of comorbidity and shared genetic risk between disorders, reflecting the pleiotropy of individual variants as well as predicted downstream pathway-level convergence. Importantly, the mechanism(s) through
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Investigating developmental and disease mechanisms of the cerebellum with pluripotent stem cells. Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-07-18 Atsushi Tamada,Shoji Watanabe,Keiko Muguruma
The cerebellum is a brain region located in the dorsal part of the anterior hindbrain, composed of a highly stereotyped neural circuit structure with small sets of neurons. The cerebellum is involved in a wide variety of functions such as motor control, learning, cognition and others. Damage to the cerebellum often leads to impairments in motor skills (cerebellar ataxia). Cerebellar ataxia can occur
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Human pluripotent stem cells: A toolbox to understand and treat retinal degeneration. Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-07-04 Lise Morizur,Elise Herardot,Christelle Monville,Karim Ben M'Barek
Age-related Macular Degeneration (AMD) and Retinitis Pigmentosa (RP) are retinal degenerative disorders that dramatically damage the retina. As there is no therapeutic option for the majority of patients, vision is progressively and irremediably lost. Owing to their unlimited renewal and potency to give rise to any cell type of the human adult body, human pluripotent stem cells (hPSCs) have been extensively
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Polysialylated - neural cell adhesion molecule (PSA-NCAM) promotes recovery of vision after the critical period. Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-07-04 Margaret Po-Shan Luke,Richard E Brown,David B Clarke
Vision loss has long since been considered irreversible after a critical period; however, there is potential to restore limited vision, even in adulthood. This phenomenon is particularly pronounced following complete loss of vision in the dominant eye. Adult neural cell adhesion molecule (NCAM) knockout mice have an age-related impairment of visual acuity. The underlying cause of early deterioration
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Timothy syndrome iPSC modeling. Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-07-03 Ramsey Bekdash,Alison D Klein,Masayuki Yazawa
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MCTP-1 modulates neurotransmitter release in C. elegans. Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-07-07 José Luis Téllez-Arreola,Malan Silva,Ataúlfo Martínez-Torres
Multiple C2 and Transmembrane Domain Proteins (MCTPs) are putative calcium sensors. Proteins that contain C2 domains play essential roles in membrane trafficking and exocytosis; however, MCTPs functions in neurotransmitter release are not known. Here we report that in C. elegans mctp-1 is under the control of two promoters - one active in the nervous system and the second in the spermatheca. We generated
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Mechanisms of axon polarization in pyramidal neurons. Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-07-10 Jyothi Arikkath
Neurons are highly polarized cells that have specialized regions for synaptic input, the dendrites, and synaptic output, the axons. This polarity is critical for appropriate neural circuit formation and function. One of the central gaps in our knowledge is understanding how developing neurons initiate axon polarity. Given the critical nature of this polarity on neural circuit formation and function
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ALS, a cellular whodunit on motor neuron degeneration. Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-07-03 Peter Karagiannis,Haruhisa Inoue
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease that primarily targets motor neurons. Motor neurons from ALS patients show cytoplasmic inclusions that are reflective of an altered RNA metabolism and protein degradation. Causal gene mutations are found in all cell types even though patient motor neurons are by far the most susceptible to the degeneration. Using induced pluripotent
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The impact of chronic stress on energy metabolism. Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-07-03 Michael A van der Kooij
The brain is exceptionally demanding in terms of energy metabolism. Approximately 20% of the calories consumed are devoted to our cerebral faculties, with the lion's share provided in the form of glucose. The brain's stringent energy dependency requires a high degree of harmonization between the elements responsible for supplying- and metabolizing energetic substrates. However, chronic stress may jeopardize
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Pharmacological inhibition of sphingosine-1-phosphate lyase partially reverses spatial memory impairment in streptozotocin-diabetic rats. Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-07-03 Urszula Baranowska,Adam Holownia,Adrian Chabowski,Marcin Baranowski
Sphingosine-1-phosphate (S1P) is a bioactive sphingolipid with strong neuroprotective properties that is important for normal excitability and synaptic transmission in the hippocampal neurons. Considering the above, the aim of the present study was to determine whether increasing brain S1P level is able to reverse spatial memory impairment in streptozotocin-diabetic rats. The experiment was carried
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Molecular mechanisms of cell polarity in a range of model systems and in migrating neurons. Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-05-30 Yves Jossin
Cell polarity is defined as the asymmetric distribution of cellular components along an axis. Most cells, from the simplest single-cell organisms to highly specialized mammalian cells, are polarized and use similar mechanisms to generate and maintain polarity. Cell polarity is important for cells to migrate, form tissues, and coordinate activities. During development of the mammalian cerebral cortex
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Tcf4 is required for correct brain development during embryogenesis. Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-05-28 Simone Mesman,Reinier Bakker,Marten P Smidt
Tcf4 has been linked to autism, schizophrenia, and Pitt-Hopkins Syndrome (PTHS) in humans, suggesting a role for Tcf4 in brain development and importantly cortical development. However, the mechanisms behind its role in disease and brain development are still elusive. We provide evidence that Tcf4 has a critical function in the differentiation of cortical regions, corpus callosum and anterior commissure
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Decoding Parkinson's disease - iPSC-derived models in the OMICs era. Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-05-18 Florian Krach,Marios-Evangelos Bogiongko,Beate Winner
Parkinson's disease (PD) is a neurodegenerative disorder characterized by the loss of dopaminergic neurons in the midbrain. In recent years, researchers have started studying PD using induced pluripotent stem cell (iPSC) models of the disease. Surprisingly, few studies have combined iPSC-technology with the so-called powerful 'omics' approaches. Here, we review the current state of omics applications
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Leptin stimulates synaptogenesis in hippocampal neurons via KLF4 and SOCS3 inhibition of STAT3 signaling. Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-05-11 Gulcan Semra Sahin,Matasha Dhar,Crystal Dillon,Mingyan Zhu,Hiroko Shiina,Bradley D Winters,Talley J Lambert,Soren Impey,Suzanne M Appleyard,Gary A Wayman
Normal development of neuronal connections in the hippocampus requires neurotrophic signals, including the cytokine leptin. During neonatal development, leptin induces formation and maturation of dendritic spines, the main sites of glutamatergic synapses in the hippocampal neurons. However, the molecular mechanisms for leptin-induced synaptogenesis are not entirely understood. In this study, we reveal
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Activation and functional modulation of satellite glial cells by oxaliplatin lead to hyperexcitability of sensory neurons in vitro. Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-05-08 Linda-Isabell Schmitt,Markus Leo,Andrea Kutritz,Christoph Kleinschnitz,Tim Hagenacker
Platinum-based chemotherapeutics still play an important role in cancer therapy, however, severe side effects, such as painful neuropathy, occur frequently. The pathophysiologic mechanisms depend on the applied chemotherapeutic agent and are still controversial. In addition to neuronal damage, disturbance of glial cell activity may contribute to neurotoxicity. Here, we focused on the effect of oxaliplatin
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Recombinant BRICHOS chaperone domains delivered to mouse brain parenchyma by focused ultrasound and microbubbles are internalized by hippocampal and cortical neurons. Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-05-08 L Galan-Acosta,C Sierra,A Leppert,A N Pouliopoulos,N Kwon,R L Noel,S Tambaro,J Presto,P Nilsson,E E Konofagou,J Johansson
The BRICHOS domain is found in human precursor proteins associated with cancer, dementia (Bri2) and amyloid lung disease (proSP-C). Recombinant human (rh) proSP-C and Bri2 BRICHOS domains delay amyloid-β peptide (Aβ) fibril formation and reduce associated toxicity in vitro and their overexpression reduces Aβ neurotoxicity in animal models of Alzheimer's disease. After intravenous administration in
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LINE-1 specific nuclear organization in mice olfactory sensory neurons. Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-05-06 Leonardo Fontoura Ormundo,Cleiton Fagundes Machado,Erika Demasceno Sakamoto,Viviane Simões,Lucia Armelin-Correa
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Effects of selective inhibition of nNOS and iNOS on neuropathic pain in rats. Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-04-27 P A Rocha,A F B Ferreira,J T Da Silva,A S Alves,D O Martins,L R G Britto,M Chacur
Various animal models have been employed to understand the pathogenic mechanism of neuropathic pain. Nitric oxide (NO) is an important molecule in nociceptive transmission and is involved in neuropathic pain. However, its mechanistic actions remain unclear. The aim of this study was to better understand the involvement of neuronal and inducible isoforms of nitric oxide synthase (nNOS and iNOS) in neuropathic
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Short-chain fatty acids (SCFAs) alone or in combination regulate select immune functions of microglia-like cells. Mol. Cell. Neurosci. (IF 3.182) Pub Date : 2020-04-22