Published by De Gruyter

Volume 29 Issue 1

Issue of Reviews in the Neurosciences

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Contents
Journal Overview

Publicly Available December 28, 2017

Frontmatter

Page range: i-iii

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September 5, 2017

Neuroinflammation and physical exercise as modulators of adult hippocampal neural precursor cell behavior

Martha Pérez-Domínguez, Luis B. Tovar-y-Romo, Angélica Zepeda

Page range: 1-20

Abstract

The dentate gyrus of the hippocampus is a plastic structure where adult neurogenesis constitutively occurs. Cell components of the neurogenic niche are source of paracrine as well as membrane-bound factors such as Notch, Bone Morphogenetic Proteins, Wnts, Sonic Hedgehog, cytokines, and growth factors that regulate adult hippocampal neurogenesis and cell fate decision. The integration and coordinated action of multiple extrinsic and intrinsic cues drive a continuous decision process: if adult neural stem cells remain quiescent or proliferate, if they take a neuronal or a glial lineage, and if new cells proliferate, undergo apoptotic death, or survive. The proper balance in the molecular milieu of this neurogenic niche leads to the production of neurons in a higher rate as that of astrocytes. But this rate changes in face of microenvironment modifications as those driven by physical exercise or with neuroinflammation. In this work, we first review the cellular and molecular components of the subgranular zone, focusing on the molecules, active signaling pathways and genetic programs that maintain quiescence, induce proliferation, or promote differentiation. We then summarize the evidence regarding the role of neuroinflammation and physical exercise in the modulation of adult hippocampal neurogenesis with emphasis on the activation of progression from adult neural stem cells to lineage-committed progenitors to their progeny mainly in murine models.

September 26, 2017

Genetic underpinnings in Alzheimer’s disease – a review

Ahmed A. Moustafa, Mubashir Hassan, Doaa H. Hewedi, Iman Hewedi, Julia K. Garami, Hany Al Ashwal, Nazar Zaki, Sung-Yum Seo, Vassilis Cutsuridis, Sergio L. Angulo, Joman Y. Natesh, Mohammad M. Herzallah, Dorota Frydecka, Błażej Misiak, Mohamed Salama, Wael Mohamed, Mohamad El Haj, Michael Hornberger

Page range: 21-38

Abstract

In this review, we discuss the genetic etiologies of Alzheimer’s disease (AD). Furthermore, we review genetic links to protein signaling pathways as novel pharmacological targets to treat AD. Moreover, we also discuss the clumps of AD-m ediated genes according to their single nucleotide polymorphism mutations. Rigorous data mining approaches justified the significant role of genes in AD prevalence. Pedigree analysis and twin studies suggest that genetic components are part of the etiology, rather than only being risk factors for AD. The first autosomal dominant mutation in the amyloid precursor protein ( APP ) gene was described in 1991. Later, AD was also associated with mutated early-onset (presenilin 1/2, PSEN1/2 and APP ) and late-onset (apolipoprotein E, ApoE ) genes. Genome-wide association and linkage analysis studies with identified multiple genomic areas have implications for the treatment of AD. We conclude this review with future directions and clinical implications of genetic research in AD.

August 21, 2017

Insights in pathogenesis of multiple sclerosis: nitric oxide may induce mitochondrial dysfunction of oligodendrocytes

Minghong Lan, Xiaoyi Tang, Jie Zhang, Zhongxiang Yao

Page range: 39-53

Abstract

Demyelinating diseases, such as multiple sclerosis (MS), are kinds of common diseases in the central nervous system (CNS), and originated from myelin loss and axonal damage. Oligodendrocyte dysfunction is the direct reason of demyelinating lesions in the CNS. Nitric oxide (NO) plays an important role in the pathological process of demyelinating diseases. Although the neurotoxicity of NO is more likely mediated by peroxynitrite rather than NO itself, NO can impair oligodendrocyte energy metabolism through mediating the damaging of mitochondrial DNA, mitochondrial membrane and mitochondrial respiratory chain complexes. In the progression of MS, NO can mainly mediate demyelination, axonal degeneration and cell death. Hence, in this review, we extensively discuss endangerments of NO in oligodendrocytes (OLs), which is suggested to be the main mediator in demyelinating diseases, e.g. MS. We hypothesize that NO takes part in MS through impairing the function of monocarboxylate transporter 1, especially causing axonal degeneration. Then, it further provides a new insight that NO for OLs may be a reliable therapeutic target to ameliorate the course of demyelinating diseases.

August 19, 2017

Computerized neurocognitive interventions in the context of the brain training controversy

Rebeca Isabel García-Betances, María Fernanda Cabrera-Umpiérrez, María T. Arredondo

Page range: 55-69

Abstract

This article presents, in the form of an analytic narrative review, a complete picture of the state-of-the-art, challenges, and perspectives in the field of information and communication technology (ICT)-based neurocognitive interventions for older adults. The narrative particularly focuses on applications aimed at mild cognitive impairment and similar age-related cognitive deficits, which are analyzed in the context of the brain training controversy. Clarifying considerations are provided about the nature and present extent of the brain training debate, regarding the possible influence it has on the support received by research and development initiatives dealing with innovative computerized neurocognitive interventions. It is recommended that, because of the preliminary nature of most data currently available in this area, further research initiatives must be supported in the quest for better effectiveness of computer-based interventions intended for age-related cognitive impairment. The conclusion suggests that advanced ICT-based tools, such as virtual and augmented reality technologies, are the most fitting platforms for applying nonpharmacological computerized neurocognitive interventions.

August 19, 2017

Vasculogenesis and angiogenesis initiation under normoxic conditions through Wnt/β-catenin pathway in gliomas

Alexandre Vallée, Rémy Guillevin, Jean-Noël Vallée

Page range: 71-91

Abstract

The canonical Wnt/β-catenin pathway is up-regulated in gliomas and involved in proliferation, invasion, apoptosis, vasculogenesis and angiogenesis. Nuclear β-catenin accumulation correlates with malignancy. Hypoxia activates hypoxia-inducible factor (HIF)-1α by inhibiting HIF-1α prolyl hydroxylation, which promotes glycolytic energy metabolism, vasculogenesis and angiogenesis, whereas HIF-1α is degraded by the HIF prolyl hydroxylase under normoxic conditions. We focus this review on the links between the activated Wnt/β-catenin pathway and the mechanisms underlying vasculogenesis and angiogenesis through HIF-1α under normoxic conditions in gliomas. Wnt-induced epidermal growth factor receptor/phosphatidylinositol 3-kinase (PI3K)/Akt signaling, Wnt-induced signal transducers and activators of transcription 3 (STAT3) signaling, and Wnt/β-catenin target gene transduction (c-Myc) can activate HIF-1α in a hypoxia-independent manner. The PI3K/Akt/mammalian target of rapamycin pathway activates HIF-1α through eukaryotic translation initiation factor 4E-binding protein 1 and STAT3. The β-catenin/T-cell factor 4 complex directly binds to STAT3 and activates HIF-1α, which up-regulates the Wnt/β-catenin target genes cyclin D1 and c-Myc in a positive feedback loop. Phosphorylated STAT3 by interleukin-6 or leukemia inhibitory factor activates HIF-1α even under normoxic conditions. The activation of the Wnt/β-catenin pathway induces, via the Wnt target genes c-Myc and cyclin D1 or via HIF-1α, gene transactivation encoding aerobic glycolysis enzymes, such as glucose transporter, hexokinase 2, pyruvate kinase M2, pyruvate dehydrogenase kinase 1 and lactate dehydrogenase-A, leading to lactate production, as the primary alternative of ATP, at all oxygen levels, even in normoxic conditions. Lactate released by glioma cells via the monocarboxylate lactate transporter-1 up-regulated by HIF-1α and lactate anion activates HIF-1α in normoxic endothelial cells by inhibiting HIF-1α prolyl hydroxylation and preventing HIF labeling by the von Hippel-Lindau protein. Increased lactate with acid environment and HIF-1α overexpression induce the vascular endothelial growth factor (VEGF) pathway of vasculogenesis and angiogenesis under normoxic conditions. Hypoxia and acidic pH have no synergistic effect on VEGF transcription.

September 22, 2017

Artemin promotes oncogenicity, metastasis and drug resistance in cancer cells

Kamal Hezam, Jiahao Jiang, Fumou Sun, Xinrong Zhang, Juan Zhang

Page range: 93-98

Abstract

Artemin (ARTN) is a member of glial cell line-derived neurotrophic factor (GDNF) family of ligands, and its signaling is mediated via a multi-component receptor complex including the glycosylphosphatidylinositol-anchored GDNF family receptors a (GFRa1, GFRa3) and RET receptor tyrosine kinase. The major mechanism of ARTN action is via binding to a non-signaling co-receptor. The major function of ARTN is to drive the molecule to induce migration and axonal projection from sympathetic neurons. It also promotes the survival, proliferation and neurite outgrowth of sympathetic neurons in vitro . ARTN triggers oncogenicity and metastasis by the activation of the AKT signaling pathway. Recent studies have reported that the expression of ARTN in hepatocellular carcinoma is associated with increased tumor size, quick relapse and shorter survival. Furthermore, ARTN promotes drug resistance such as antiestrogens, doxorubicin, fulvestrant, paclitaxel, tamoxifen and trastuzumab. Moreover, ARTN also stimulates the radio-therapeutic resistance. This review highlights the proposed roles of ARTN in cancer cells and discusses recent results supporting its emerging role as an oncogenic, metastatic and drug-resisting agent with a special focus on how these new insights may facilitate rational development of ARTN for targeted therapies in the future.

August 18, 2017

The effects of transcranial direct current stimulation on short-interval intracortical inhibition and intracortical facilitation: a systematic review and meta-analysis

Mana Biabani, Maryam Aminitehrani, Maryam Zoghi, Michael Farrell, Gary Egan, Shapour Jaberzadeh

Page range: 99-114

Abstract

Transcranial direct current stimulation (tDCS) is increasingly being used to affect the neurological conditions with deficient intracortical synaptic activities (i.e. Parkinson’s disease and epilepsy). In addition, it is suggested that the lasting effects of tDCS on corticospinal excitability (CSE) have intracortical origin. This systematic review and meta-analysis aimed to examine whether tDCS has any effect on intracortical circuits. Eleven electronic databases were searched for the studies investigating intracortical changes induced by anodal (a) and cathodal (c) tDCS, in healthy individuals, using two paired-pulse transcranial magnetic stimulation (TMS) paradigms: short-interval intracortical inhibition (SICI) and intracortical facilitation (ICF). Additionally, motor-evoked potential (MEP) size alterations, assessed by single-pulse TMS, were extracted from these studies to investigate the probable intracortical origin of tDCS effects on CSE. The methodological quality of included studies was examined using Physiotherapy Evidence Database (PEDro) and Downs and Black’s (D&B) assessment tools. Thirteen research papers, including 24 experiments, were included in this study scoring good and medium quality in PEDro and D&B scales, respectively. Immediately following anodal tDCS (a-tDCS) applications, we found significant decreases in SICI, but increases in ICF and MEP size. However, ICF and MEP size significantly decreased, and SICI increased immediately following cathodal tDCS (c-tDCS). The results of this systematic review and meta-analysis reveal that a-tDCS changes intracortical activities (SICI and ICF) toward facilitation, whereas c-tDCS alters them toward inhibition. It can also be concluded that increases and decreases in CSE after tDCS application are associated with corresponding changes in intracortical activities. The results suggest that tDCS can be clinically useful to modulate intracortical circuits.

About this journal

Reviews in the Neurosciences provides a forum for reviews, critical evaluations and theoretical treatment of selective topics in the neurosciences. The journal is meant to provide an authoritative reference work for those interested in the structure and functions of the nervous system at all levels of analysis, including the genetic, molecular, cellular, behavioral, cognitive and clinical neurosciences. Contributions should contain a critical appraisal of specific areas and not simply a compilation of published articles.

Previously published by Freund Publishing House Ltd.

Topics

Neurology
Psychiatry
Neuropharmacology
Neurochemistry
Neurophysiology
Behavioral Psychology
Pharmacology
Neuroanatomy

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