265 results match your criteria ASN neuro[Journal]


Astrocyte and Neuronal Pannexin1 Contribute Distinctly to Seizures.

ASN Neuro 2019 Jan-Dec;11:1759091419833502

1 Department of Cell Biology and Anatomy, New York Medical College, Valhalla, NY, USA.

ATP- and adenosine-mediated signaling are prominent types of glia-glia and glia-neuron interaction, with an imbalance of ATP/adenosine ratio leading to altered states of excitability, as seen in epileptic seizures. Pannexin1 (Panx1), a member of the gap junction family, is an ATP release channel that is expressed in astrocytes and neurons. Previous studies provided evidence supporting a role for purinergic-mediated signaling via Panx1 channels in seizures; using mice with global deletion of Panx1, it was shown that these channels contribute in maintenance of seizures by releasing ATP. Read More

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http://dx.doi.org/10.1177/1759091419833502DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6415468PMC

Sildenafil Inhibits Myelin Expression and Myelination of Oligodendroglial Precursor Cells.

ASN Neuro 2019 Jan-Dec;11:1759091419832444

1 Laboratory of Neuroimmunoendocrinology, National Institute of Neurology and Neurosurgery Manuel Velasco Suarez, Mexico.

Phosphodiesterases (PDEs) have previously been implicated in oligodendrocyte maturation and myelination of central nervous system axons. Sildenafil citrate is a phosphodiesterase inhibitor known to block PDE5, which also reduces inflammation in the experimental autoimmune encephalomyelitis demyelinating model. To find out whether this inhibitor might exert beneficial effects on central nervous system myelin repair activities, we investigated to what degree sildenafil modulates differentiation and maturation of cultured primary rat oligodendroglial precursor cells (OPCs). Read More

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http://dx.doi.org/10.1177/1759091419832444DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6410393PMC
March 2019
2 Reads

Subacute Transplantation of Native and Genetically Engineered Neural Progenitors Seeded on Microsphere Scaffolds Promote Repair and Functional Recovery After Traumatic Brain Injury.

ASN Neuro 2019 Jan-Dec;11:1759091419830186

3 Department of Biological Sciences, Rutgers University, Newark, NJ, USA.

There is intense interest and effort toward regenerating the brain after severe injury. Stem cell transplantation after insult to the central nervous system has been regarded as the most promising approach for repair; however, engrafting cells alone might not be sufficient for effective regeneration. In this study, we have compared neural progenitors (NPs) from the fetal ventricular zone (VZ), the postnatal subventricular zone, and an immortalized radial glia (RG) cell line engineered to conditionally secrete the trophic factor insulin-like growth factor 1 (IGF-1). Read More

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http://dx.doi.org/10.1177/1759091419830186DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6399762PMC

A Longitudinal Investigation of Sleep and Daytime Wakefulness in Children and Youth With Concussion.

ASN Neuro 2019 Jan-Dec;11:1759091418822405

6 Montreal Children's Hospital, McGill University Health Center, Montreal, Québec, Canada.

A high proportion of adults who sustain a concussion identify changes in their sleep during the acute stage, typically reporting an increased need for sleep or nonrestful sleep. Our understanding of sleep following concussion is less well understood within a pediatric population. In this study, we investigated the trajectory of sleep and daytime sleepiness in a prospective cohort of 40 children and youth (6-18 years old) with concussion, 40 age-and sex-matched healthy children and youth, and 40 with upper-extremity orthopedic injury. Read More

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http://journals.sagepub.com/doi/10.1177/1759091418822405
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http://dx.doi.org/10.1177/1759091418822405DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6343438PMC
February 2019
5 Reads

α-Synuclein Trafficking in Parkinson's Disease: Insights From Fly and Mouse Models.

ASN Neuro 2018 Jan-Dec;10:1759091418812587

1 School of Life Science and Technology, ShanghaiTech University, Shanghai, China.

Protein aggregation and accumulation are common pathological hallmarks in neurodegenerative diseases. To efficiently clear and eliminate such aggregation becomes an important cellular strategy for cell survival. Lewy bodies inclusion and aggregation of α-Synuclein (α-Syn) during the pathogenesis of Parkinson's disease (PD) serve as a good example and are potentially linked to other pathological PD features such as progressive dopaminergic neuron cell death, behavioral defects, and nonmotor symptoms like anosmia, cognitive impairment, and depression. Read More

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http://dx.doi.org/10.1177/1759091418812587DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6259071PMC
November 2018

L-DOPA-Induced Motor Impairment and Overexpression of Corticostriatal Synaptic Components Are Improved by the mGluR5 Antagonist MPEP in 6-OHDA-Lesioned Rats.

ASN Neuro 2018 Jan-Dec;10:1759091418811021

1 Department of Neurology, The Second Affiliated Hospital of Soochow University, Suzhou, China.

Levodopa (L-DOPA) is still the most effective drug for the treatment of Parkinson's disease (PD). However, the long-term therapy often triggers L-DOPA-induced dyskinesia (LID). Metabotropic glutamate receptor type 5 (mGluR5) is abundant in the basal ganglia, and its inhibition is thought to modulate postsynaptic excitatory synaptic transmission and glutamate hyperactivity in PD and LID. Read More

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http://journals.sagepub.com/doi/10.1177/1759091418811021
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http://dx.doi.org/10.1177/1759091418811021DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6238196PMC
November 2018
2 Reads

Neuroprotective Effect of Nortriptyline in Overt Hepatic Encephalopathy Through Attenuation of Mitochondrial Dysfunction.

ASN Neuro 2018 Jan-Dec;10:1759091418810583

1 Department of Anatomy, College of Medicine, Konyang University, Daejeon, South Korea.

Hyperammonemia associated with overt hepatic encephalopathy (OHE) causes excitotoxic neuronal death through activation of the cytochrome C (CytC)-mediated mitochondria-dependent apoptotic pathway. We tested the therapeutic effect of nortriptyline (NT), a mitochondrial permeability transition pore (mPTP) blocker that can possibly inhibit mitochondrial CytC efflux to the cytosol on in vivo and in vitro OHE models. After ensuring the generation of OHE rats, established by bile duct ligation (BDL), they were intraperitoneally administered either 20 mg/kg NT (i. Read More

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http://journals.sagepub.com/doi/10.1177/1759091418810583
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http://dx.doi.org/10.1177/1759091418810583DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6238202PMC
November 2018
22 Reads

An In Vitro Model of Charcot-Marie-Tooth Disease Type 4B2 Provides Insight Into the Roles of MTMR13 and MTMR2 in Schwann Cell Myelination.

ASN Neuro 2018 Jan-Dec;10:1759091418803282

1 Department of Neurology, Jungers Center for Neurosciences Research, Oregon Health & Science University, Portland, OR, USA.

Charcot-Marie-Tooth Disorder Type 4B (CMT4B) is a demyelinating peripheral neuropathy caused by mutations in myotubularin-related (MTMR) proteins 2, 13, or 5 (CMT4B1/2/3), which regulate phosphoinositide turnover and endosomal trafficking. Although mouse models of CMT4B2 exist, an in vitro model would make possible pharmacological and reverse genetic experiments needed to clarify the role of MTMR13 in myelination. We have generated such a model using Schwann cell-dorsal root ganglion (SC-DRG) explants from Mtmr13 mice. Read More

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http://journals.sagepub.com/doi/10.1177/1759091418803282
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http://dx.doi.org/10.1177/1759091418803282DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6236487PMC
November 2018
10 Reads

Sensory Processing Phenotypes in Fragile X Syndrome.

ASN Neuro 2018 Jan-Dec;10:1759091418801092

1 Division of Biomedical Sciences, University of California Riverside School of Medicine, CA, USA.

Fragile X syndrome (FXS) is a neurodevelopmental disorder that causes intellectual disability. It is a leading known genetic cause of autism. In addition to cognitive, social, and communication deficits, humans with FXS demonstrate abnormal sensory processing including sensory hypersensitivity. Read More

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http://dx.doi.org/10.1177/1759091418801092DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6149018PMC
September 2018
3 Reads

Continuous Inhalation Exposure to Fungal Allergen Particulates Induces Lung Inflammation While Reducing Innate Immune Molecule Expression in the Brainstem.

ASN Neuro 2018 Jan-Dec;10:1759091418782304

1 BREATHE Center, University of California, Riverside, CA, USA.

Continuous exposure to aerosolized fine (particle size ≤2.5 µm) and ultrafine (particle size ≤0.1 µm) particulates can trigger innate inflammatory responses in the lung and brain depending on particle composition. Read More

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http://dx.doi.org/10.1177/1759091418782304DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6053578PMC
July 2018
4 Reads

Alternative Method to Detect Neuronal Degeneration and Amyloid β Accumulation in Free-Floating Brain Sections With Fluoro-Jade.

ASN Neuro 2018 Jan-Dec;10:1759091418784357

1 Department of Pharmacology, School of Medicine, Universidad Complutense de Madrid (UCM), Spain.

Fluoro-Jade is a fluorescein-derived fluorochrome which specifically binds to damaged neurons. Due to this characteristic, it is commonly used for the histochemical detection and quantification of neurodegeneration in mounted brain sections. Here, we describe an alternative and simpler histochemistry protocol based on the use of free-floating brain sections. Read More

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http://dx.doi.org/10.1177/1759091418784357DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6043921PMC
June 2018
7 Reads

Repeated Mild Closed Head Injuries Induce Long-Term White Matter Pathology and Neuronal Loss That Are Correlated With Behavioral Deficits.

ASN Neuro 2018 Jan-Dec;10:1759091418781921

1 Department of Anatomy and Neurobiology, University of California-Irvine, CA, USA.

An estimated 5.3 million Americans are living with a disability from a traumatic brain injury (TBI). There is emerging evidence of the detrimental effects from repeated mild TBIs (rmTBIs). Read More

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http://dx.doi.org/10.1177/1759091418781921DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6050992PMC
June 2018
10 Reads

Sex-Related Abnormalities in Substantia Nigra Lipids in Parkinson's Disease.

ASN Neuro 2018 Jan-Dec;10:1759091418781889

2 Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia, PA, USA.

Parkinson's disease (PD) is a neurodegenerative movement disorder involving the selective loss of dopamine-producing neurons in the substantia nigra (SN). Differences in disease presentation, prevalence, and age of onset have been reported between males and females with PD. The content and composition of the major glycosphingolipids, phospholipids, and cholesterol were evaluated in the SN from 12 PD subjects and in 18 age-matched, neurologically normal controls. Read More

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http://dx.doi.org/10.1177/1759091418781889DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6024349PMC
June 2018
1 Read

Overexpression of CLEC18B Associates With the Proliferation, Migration, and Prognosis of Glioblastoma.

ASN Neuro 2018 Jan-Dec;10:1759091418781949

1 Department of Neurosurgery, The First Affiliated Hospital of Zhengzhou University, Henan, P.R. China.

C-type lectin domain family 18 member B (CLEC18B), encoding a superfamily of CLEC, has been found to be expressed in some of cancer cells, which possibly indicates it associated with cancer. However, the defined functional characterizations of CLEC18B in glioblastoma multiforme (GBM) progression still remain unclear. To this end, clinical relevance of CLEC18B expression with GBM patients' prognosis was analyzed both in The Cancer Genome Atlas dataset of 174 tissues and 40 GBM tumor tissues collected from our hospital by using the Kaplan-Meier survival and the Cox proportional hazard model. Read More

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http://dx.doi.org/10.1177/1759091418781949DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6024345PMC
June 2018
4 Reads

Neurotoxin-Induced Animal Models of Parkinson Disease: Pathogenic Mechanism and Assessment.

ASN Neuro 2018 Jan-Dec;10:1759091418777438

1 College of Life Sciences, Institute for Conservation and Utilization of Agro-Bioresources in Dabie Mountains, Xinyang Normal University, China.

Parkinson disease (PD) is the second most common neurodegenerative movement disorder. Pharmacological animal models are invaluable tools to study the pathological mechanisms of PD. Currently, invertebrate and vertebrate animal models have been developed by using several main neurotoxins, such as 6-hydroxydopamine, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, paraquat, and rotenone. Read More

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http://dx.doi.org/10.1177/1759091418777438DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5977437PMC

In Vivo Optical Imaging of Myelination Events in a Myelin Basic Protein Promoter-Driven Luciferase Transgenic Mouse Model.

ASN Neuro 2018 Jan-Dec;10:1759091418777329

1 Translational In Vivo Model, Global Research Platform, Sanofi R&D, Framingham, MA, USA.

The compact myelin sheath is important for axonal function, and its loss can lead to neuronal cell death and irreversible functional deficits. Myelin is vulnerable to a variety of metabolic, toxic, and autoimmune insults. In diseases like multiple sclerosis, there is currently no therapy to stop myelin loss, underscoring the need for neuroprotective and remyelinating therapies. Read More

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http://dx.doi.org/10.1177/1759091418777329DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5987236PMC
May 2018
11 Reads

Neuroprotective Role of Astroglia in Parkinson Disease by Reducing Oxidative Stress Through Dopamine-Induced Activation of Pentose-Phosphate Pathway.

ASN Neuro 2018 Jan-Dec;10:1759091418775562

1 Department of Neurology, Keio University School of Medicine, Tokyo, Japan.

Oxidative stress plays an important role in the onset and progression of Parkinson disease. Although released dopamine at the synaptic terminal is mostly reabsorbed by dopaminergic neurons, some dopamine is presumably taken up by astroglia. This study examined the dopamine-induced astroglial protective function through the activation of the pentose-phosphate pathway (PPP) to reduce reactive oxygen species (ROS). Read More

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http://journals.sagepub.com/doi/10.1177/1759091418775562
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http://dx.doi.org/10.1177/1759091418775562DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5960859PMC
May 2018
14 Reads

Metabolic and Structural Imaging at 7 Tesla After Repetitive Mild Traumatic Brain Injury in Immature Rats.

ASN Neuro 2018 Jan-Dec;10:1759091418770543

1 Safar Center for Resuscitation Research, Department of Critical Care Medicine, University of Pittsburgh, PA, USA.

Mild traumatic brain injury (mTBI) in children is a common and serious public health problem. Traditional neuroimaging findings in children who sustain mTBI are often normal, putting them at risk for repeated mTBI (rmTBI). There is a need for more sensitive imaging techniques capable of detecting subtle neurophysiological alterations after injury. Read More

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http://journals.sagepub.com/doi/10.1177/1759091418770543
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http://dx.doi.org/10.1177/1759091418770543DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5944144PMC
May 2018
8 Reads

Methylglyoxal Disrupts Paranodal Axoglial Junctions via Calpain Activation.

ASN Neuro 2018 Jan-Dec;10:1759091418766175

1 Department of Neuroscience, Cell Biology, and Physiology, Boonshoft School of Medicine, Wright State University, Dayton, OH, USA.

Nodes of Ranvier and associated paranodal and juxtaparanodal domains along myelinated axons are essential for normal function of the peripheral and central nervous systems. Disruption of these domains as well as increases in the reactive carbonyl species methylglyoxal are implicated as a pathophysiology common to a wide variety of neurological diseases. Here, using an ex vivo nerve exposure model, we show that increasing methylglyoxal produces paranodal disruption, evidenced by disorganized immunostaining of axoglial cell-adhesion proteins, in both sciatic and optic nerves from wild-type mice. Read More

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http://dx.doi.org/10.1177/1759091418766175DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5944142PMC
April 2018
5 Reads

Corrigendum.

Authors:

ASN Neuro 2018 Jan-Dec;10:1759091417752571

Lavezzi, A. M., Ferrero, S. Read More

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http://dx.doi.org/10.1177/1759091417752571DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5896843PMC
January 2018
1 Read

Stuck in a State of Inattention? Functional Hyperconnectivity as an Indicator of Disturbed Intrinsic Brain Dynamics in Adolescents With Concussion: A Pilot Study.

ASN Neuro 2018 Jan-Dec;10:1759091417753802

1 Department of Physical Therapy, Faculty of Medicine, University of British Columbia, Vancouver, BC, Canada.

Sports-related concussion in youth is a major public health issue. Evaluating the diffuse and often subtle changes in structure and function that occur in the brain, particularly in this population, remains a significant challenge. The goal of this pilot study was to evaluate the relationship between the intrinsic dynamics of the brain using resting-state functional magnetic resonance imaging (rs-fMRI) and relate these findings to structural brain correlates from diffusion tensor imaging in a group of adolescents with sports-related concussions ( n = 6) and a group of healthy adolescent athletes ( n = 6). Read More

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http://dx.doi.org/10.1177/1759091417753802DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5784460PMC
January 2018
2 Reads

Mitochondrial Substrate-Level Phosphorylation as Energy Source for Glioblastoma: Review and Hypothesis.

ASN Neuro 2018 Jan-Dec;10:1759091418818261

2 Biology Department, Boston College, Chestnut Hill, MA, USA.

Glioblastoma multiforme (GBM) is the most common and malignant of the primary adult brain cancers. Ultrastructural and biochemical evidence shows that GBM cells exhibit mitochondrial abnormalities incompatible with energy production through oxidative phosphorylation (OxPhos). Under such conditions, the mitochondrial F0-F1 ATP synthase operates in reverse at the expense of ATP hydrolysis to maintain a moderate membrane potential. Read More

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http://dx.doi.org/10.1177/1759091418818261DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6311572PMC

Iron Deficiency Affects Seizure Susceptibility in a Time- and Sex-Specific Manner.

ASN Neuro 2017 Nov-Dec;9(6):1759091417746521

2 Department of Biomedical Genetics, University of Rochester, NY, USA.

Iron deficiency (ID) affects more than three billion people worldwide making it the most common micronutrient deficiency. ID is most prevalent during gestation and early life, which is of particular concern since its impact on the developing central nervous system is associated with an increased risk of a wide range of different psychiatric disorders later in life. The cause for this association is not known, but many of these same disorders are also associated with an imbalance between excitation and inhibition (E/I) within the brain. Read More

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http://dx.doi.org/10.1177/1759091417746521DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5734468PMC
July 2018
1 Read

Oxidative Stress Induces Disruption of the Axon Initial Segment.

ASN Neuro 2017 Nov-Dec;9(6):1759091417745426

1 Department of Anatomy and Neurobiology, 72054 Virginia Commonwealth University , Richmond, VA, USA.

The axon initial segment (AIS), the domain responsible for action potential initiation and maintenance of neuronal polarity, is targeted for disruption in a variety of central nervous system pathological insults. Previous work in our laboratory implicates oxidative stress as a potential mediator of structural AIS alterations in two separate mouse models of central nervous system inflammation, as these effects were attenuated following reactive oxygen species scavenging and NADPH oxidase-2 ablation. While these studies suggest a role for oxidative stress in modulation of the AIS, the direct effects of reactive oxygen and nitrogen species (ROS/RNS) on the stability of this domain remain unclear. Read More

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http://dx.doi.org/10.1177/1759091417745426DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5734465PMC
July 2018
2 Reads

Hyperhomocysteinemia-Induced Gene Expression Changes in the Cell Types of the Brain.

ASN Neuro 2017 Nov-Dec;9(6):1759091417742296

1 Sanders-Brown Center on Aging, University of Kentucky, Lexington, KY, USA.

High plasma levels of homocysteine, termed hyperhomocysteinemia, are a risk factor for vascular cognitive impairment and dementia, which is the second leading cause of dementia. While hyperhomocysteinemia induces microhemorrhages and cognitive decline in mice, the specific effect of hyperhomocysteinemia on each cell type remains unknown. We took separate cultures of astrocytes, microglia, endothelial cells, and neuronal cells and treated each with moderate levels of homocysteine for 24, 48, 72, and 96 hr. Read More

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http://dx.doi.org/10.1177/1759091417742296DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5718317PMC
July 2018
4 Reads

Tissue Inhibitor of Metalloproteinase-3 Promotes Schwann Cell Myelination.

ASN Neuro 2017 Nov-Dec;9(6):1759091417745425

1 Department of Biological Sciences, 169278 Rutgers University , Newark, NJ, USA.

Tissue inhibitor of metalloproteinase-3 (TIMP-3) inhibits the activities of various metalloproteinases including matrix metalloproteinases and ADAM family proteins. In the peripheral nervous system, ADAM17, also known as TNF-α converting enzyme (TACE), cleaves the extracellular domain of Nrg1 type III, an axonal growth factor that is essential for Schwann cell myelination. The processing by ADAM17 attenuates Nrg1 signaling and inhibits Schwann cell myelination. Read More

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http://dx.doi.org/10.1177/1759091417745425DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5718315PMC
July 2018
10 Reads

Mitogen- and Stress-Activated Protein Kinase 1 Regulates Status Epilepticus-Evoked Cell Death in the Hippocampus.

ASN Neuro 2017 Sep-Oct;9(5):1759091417726607

2 Department of Neuroscience, 2647 Ohio State University , Columbus, OH, USA.

Mitogen-activated protein kinase (MAPK) signaling has been implicated in a wide range of neuronal processes, including development, plasticity, and viability. One of the principal downstream targets of both the extracellular signal-regulated kinase/MAPK pathway and the p38 MAPK pathway is Mitogen- and Stress-activated protein Kinase 1 (MSK1). Here, we sought to understand the role that MSK1 plays in neuroprotection against excitotoxic stimulation in the hippocampus. Read More

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http://journals.sagepub.com/doi/10.1177/1759091417726607
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http://dx.doi.org/10.1177/1759091417726607DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5588809PMC
May 2018
11 Reads

An Alternative Cuprizone-Induced Demyelination and Remyelination Mouse Model.

ASN Neuro 2017 Jul-Aug;9(4):1759091417725174

1 Department of Integrated Biological Platform Sciences, GlaxoSmithKline, R&D China, Shanghai, China.

The cuprizone model is a well-established and investigated paradigm to study demyelination and remyelination in rodents. Cuprizone is usually administrated by mixing in the powdered or pelleted rodent chow. However, since cuprizone is sensitive to the environment and the consumption of it varies between different animals, the major issue is the discrepancy in demyelination of the animals. Read More

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http://dx.doi.org/10.1177/1759091417725174DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5574485PMC
December 2017
12 Reads

Dissecting Amyloid Beta Deposition Using Distinct Strains of the Neurotropic Parasite Toxoplasma gondii as a Novel Tool.

ASN Neuro 2017 Jul-Aug;9(4):1759091417724915

1 BIO5 Institute, 8041 University of Arizona , Tucson, AZ, USA.

Genetic and pathologic data suggest that amyloid beta (Aβ), produced by processing of the amyloid precursor protein, is a major initiator of Alzheimer's disease (AD). To gain new insights into Aβ modulation, we sought to harness the power of the coevolution between the neurotropic parasite Toxoplasma gondii and the mammalian brain. Two prior studies attributed Toxoplasma-associated protection against Aβ to increases in anti-inflammatory cytokines (TGF-β and IL-10) and infiltrating phagocytic monocytes. Read More

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http://dx.doi.org/10.1177/1759091417724915DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5565021PMC
December 2017
11 Reads

Effects of Intron 1 Sequences on Human PLP1 Expression: Implications for PLP1-Related Disorders.

Authors:
Patricia A Wight

ASN Neuro 2017 Jul-Aug;9(4):1759091417720583

1 Department of Physiology and Biophysics, University of Arkansas for Medical Sciences, Little Rock, AR, USA.

Alterations in the myelin proteolipid protein gene ( PLP1) may result in rare X-linked disorders in humans such as Pelizaeus-Merzbacher disease and spastic paraplegia type 2. PLP1 expression must be tightly regulated since null mutations, as well as elevated PLP1 copy number, both lead to disease. Previous studies with Plp1-lacZ transgenic mice have demonstrated that mouse Plp1 ( mPlp1) intron 1 DNA (which accounts for slightly more than half of the gene) is required for the mPlp1 promoter to drive significant levels of reporter gene expression in brain. Read More

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http://journals.sagepub.com/doi/10.1177/1759091417720583
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http://dx.doi.org/10.1177/1759091417720583DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5528184PMC
December 2017
3 Reads

Nicotinic Receptor Abnormalities in the Cerebellar Cortex of Sudden Unexplained Fetal and Infant Death Victims-Possible Correlation With Maternal Smoking.

ASN Neuro 2017 Jul-Aug;9(4):1759091417720582

4 Department of Diagnostic and Clinical Medicine and of Public Health, Section of Pathology, University of Modena and Reggio Emilia, Policlinico Hospital, Modena, Italy.

Nicotinic acetylcholine receptors (nAChRs) are cationic channels of the neuronal cell membrane, differentially expressed in the central nervous system which, when activated by endogenous acetylcholine or exogenous nicotine, are able to enhance cholinergic transmission. The aim of this study was to investigate in human perinatal age the immunohistochemical expression of the α7-nAChR subtype, given its involvement in neuronal differentiation and its significant vulnerability to the toxic effects of nicotine. Thirty fetuses (with a gestational age between 25 and 40 weeks) and 35 infants (1-6 months old), suddenly died of known (controls) and unknown causes (unexplained deaths), with smoking and nonsmoking mothers, were included in this study. Read More

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http://journals.sagepub.com/doi/10.1177/1759091417720582
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http://dx.doi.org/10.1177/1759091417720582DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5528189PMC
December 2017
12 Reads

Peripheral Inflammation, Apolipoprotein E4, and Amyloid-β Interact to Induce Cognitive and Cerebrovascular Dysfunction.

ASN Neuro 2017 Jul-Aug;9(4):1759091417719201

1 Department of Anatomy and Cell Biology, University of Illinois at Chicago, IL, USA.

Cerebrovascular dysfunction is rapidly reemerging as a major process of Alzheimer's disease (AD). It is, therefore, crucial to delineate the roles of AD risk factors in cerebrovascular dysfunction. While apolipoprotein E4 ( APOE4), Amyloid-β (Aβ), and peripheral inflammation independently induce cerebrovascular damage, their collective effects remain to be elucidated. Read More

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http://dx.doi.org/10.1177/1759091417719201DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5521356PMC
December 2017
23 Reads

Modulation of Hematopoietic Lineage Specification Impacts TREM2 Expression in Microglia-Like Cells Derived From Human Stem Cells.

ASN Neuro 2017 Jul-Aug;9(4):1759091417716610

1 Department of Neurology, University of Washington, Seattle, WA, USA.

Microglia are the primary innate immune cell type in the brain, and their dysfunction has been linked to a variety of central nervous system disorders. Human microglia are extraordinarily difficult to obtain for experimental investigation, limiting our ability to study the impact of human genetic variants on microglia functions. Previous studies have reported that microglia-like cells can be derived from human monocytes or pluripotent stem cells. Read More

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http://dx.doi.org/10.1177/1759091417716610DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5548325PMC
December 2017
32 Reads

Cortical Plasticity in Depression.

ASN Neuro 2017 May-Jun;9(3):1759091417711512

5 Department of Medical and Surgical Sciences and Advanced Technology, Section of Neurosciences, University of Catania, Catania, Italy.

Neural plasticity is considered the neurophysiological correlate of learning and memory, although several studies have also noted that it plays crucial roles in a number of neurological and psychiatric diseases. Indeed, impaired brain plasticity may be one of the pathophysiological mechanisms that underlies both cognitive decline and major depression. Moreover, a degree of cognitive impairment is frequently observed throughout the clinical spectrum of mood disorders, and the relationship between depression and cognition is often bidirectional. Read More

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http://dx.doi.org/10.1177/1759091417711512DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5480639PMC
December 2017
10 Reads

Heterogeneity of D-Serine Distribution in the Human Central Nervous System.

ASN Neuro 2017 May-Jun;9(3):1759091417713905

1 Department of Anatomy, Keio University School of Medicine, Tokyo, Japan.

D-serine is an endogenous ligand for N-methyl-D-aspartate glutamate receptors. Accumulating evidence including genetic associations of D-serine metabolism with neurological or psychiatric diseases suggest that D-serine is crucial in human neurophysiology. However, distribution and regulation of D-serine in humans are not well understood. Read More

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http://dx.doi.org/10.1177/1759091417713905DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5470653PMC
December 2017
9 Reads

PACAP Promotes Matrix-Driven Adhesion of Cultured Adult Murine Neural Progenitors.

ASN Neuro 2017 May-Jun;9(3):1759091417708720

1 Intellectual Development and Disabilities Research Center, The David Geffen School of Medicine, University of California, Los Angeles, CA, USA.

New neurons are born throughout the life of mammals in germinal zones of the brain known as neurogenic niches: the subventricular zone of the lateral ventricles and the subgranular zone of the dentate gyrus of the hippocampus. These niches contain a subpopulation of cells known as adult neural progenitor cells (aNPCs), which self-renew and give rise to new neurons and glia. aNPCs are regulated by many factors present in the niche, including the extracellular matrix (ECM). Read More

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http://dx.doi.org/10.1177/1759091417708720DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5439654PMC
December 2017
35 Reads

Conditional Depletion of Hippocampal Brain-Derived Neurotrophic Factor Exacerbates Neuropathology in a Mouse Model of Alzheimer's Disease.

ASN Neuro 2017 Mar-Apr;9(2):1759091417696161

2 Jesse Brown VA Medical Center, Chicago, IL, USA.

Damage occurring to noradrenergic neurons in the locus coeruleus (LC) contributes to the evolution of neuroinflammation and neurodegeneration in a variety of conditions and diseases. One cause of LC damage may be loss of neurotrophic support from LC target regions. We tested this hypothesis by conditional unilateral knockout of brain-derived neurotrophic factor (BDNF) in adult mice. Read More

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http://dx.doi.org/10.1177/1759091417696161DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5415058PMC
October 2017
3 Reads

Loss of Interneuron-Derived Collagen XIX Leads to a Reduction in Perineuronal Nets in the Mammalian Telencephalon.

ASN Neuro 2017 Feb;9(1):1759091416689020

1 Virginia Tech Carilion Research Institute, Roanoke, VA, USA.

Perineuronal nets (PNNs) are lattice-like supramolecular assemblies of extracellular glycoproteins that surround subsets of neuronal cell bodies in the mammalian telencephalon. PNNs emerge at the end of the critical period of brain development, limit neuronal plasticity in the adult brain, and are lost in a variety of complex brain disorders diseases, including schizophrenia. The link between PNNs and schizophrenia led us to question whether neuronally expressed extracellular matrix (ECM) molecules associated with schizophrenia contribute to the assembly of these specialized supramolecular ECM assemblies. Read More

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http://dx.doi.org/10.1177/1759091416689020DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5298462PMC
February 2017

Unaltered Glutamate Transporter-1 Protein Levels in Aquaporin-4 Knockout Mice.

ASN Neuro 2017 Feb;9(1):1759091416687846

1 Center for Glial-Neuronal Interactions, Division of Biomedical Sciences, University of California, Riverside, CA, USA.

Maintenance of glutamate and water homeostasis in the brain is crucial to healthy brain activity. Astrocytic glutamate transporter-1 (GLT1) and aquaporin-4 (AQP4) are the main regulators of extracellular glutamate and osmolarity, respectively. Several studies have reported colocalization of GLT1 and AQP4, but the existence of a physical interaction between the two has not been well studied. Read More

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http://dx.doi.org/10.1177/1759091416687846DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5315234PMC
February 2017

C5a Increases the Injury to Primary Neurons Elicited by Fibrillar Amyloid Beta.

ASN Neuro 2017 Feb;9(1):1759091416687871

1 Department of Pathology and Laboratory Medicine, University of California, Irvine, School of Medicine, Irvine, USA.

C5aR1, the proinflammatory receptor for C5a, is expressed in the central nervous system on microglia, endothelial cells, and neurons. Previous work demonstrated that the C5aR1 antagonist, PMX205, decreased amyloid pathology and suppressed cognitive deficits in two Alzheimer's Disease (AD) mouse models. However, the cellular mechanisms of this protection have not been definitively demonstrated. Read More

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http://dx.doi.org/10.1177/1759091416687871DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5298486PMC
February 2017
1 Read

NCAM1 Polysialylation: The Prion Protein's Elusive Reason for Being?

ASN Neuro 2016 12 22;8(6). Epub 2016 Nov 22.

Tanz Centre for Research in Neurodegenerative Diseases, University of Toronto, Toronto, Ontario, Canada

Much confusion surrounds the physiological function of the cellular prion protein (PrP). It is, however, anticipated that knowledge of its function will shed light on its contribution to neurodegenerative diseases and suggest ways to interfere with the cellular toxicity central to them. Consequently, efforts to elucidate its function have been all but exhaustive. Read More

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http://dx.doi.org/10.1177/1759091416679074DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5122176PMC
December 2016
4 Reads

HIV Glycoprotein Gp120 Impairs Fast Axonal Transport by Activating Tak1 Signaling Pathways.

ASN Neuro 2016 12 20;8(6). Epub 2016 Nov 20.

Department of Anatomy and Cell Biology, University of Illinois at Chicago, IL, USA

Sensory neuropathies are the most common neurological complication of HIV. Of these, distal sensory polyneuropathy (DSP) is directly caused by HIV infection and characterized by length-dependent axonal degeneration of dorsal root ganglion (DRG) neurons. Mechanisms for axonal degeneration in DSP remain unclear, but recent experiments revealed that the HIV glycoprotein gp120 is internalized and localized within axons of DRG neurons. Read More

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http://dx.doi.org/10.1177/1759091416679073DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5119683PMC
December 2016
5 Reads

Assessment of Neuroprotective Properties of Melissa officinalis in Combination With Human Umbilical Cord Blood Stem Cells After Spinal Cord Injury.

ASN Neuro 2016 10 3;8(6). Epub 2016 Nov 3.

Neuroscience Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran.

Introduction: The pathophysiology of spinal cord injury (SCI) has a classically bad prognosis. It has been demonstrated that human umbilical cord blood stem cells (hUCBSCs) and Melissa officinalis (MO) are useful for the prevention of neurological disease.

Methods: Thirty-six adult male rats were randomly divided into intact, sham, control (SCI), MO, hUCBSC, and MO-hUCBSC groups. Read More

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http://dx.doi.org/10.1177/1759091416674833DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5098695PMC
October 2016
3 Reads

Grafted Neural Precursors Integrate Into Mouse Striatum, Differentiate and Promote Recovery of Function Through Release of Erythropoietin in MPTP-Treated Mice.

ASN Neuro 2016 10 27;8(5). Epub 2016 Oct 27.

Laboratories of Pharmacology, Department of Health Sciences, University of Milan, Italy.

Erythropoietin-releasing neural precursor cells (Er-NPCs) are a subclass of subventricular zone-derived neural progenitors, capable of surviving for 6 hr after death of donor. They present higher neural differentiation. Here, Er-NPCs were studied in animal model of Parkinson's disease. Read More

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http://dx.doi.org/10.1177/1759091416676147DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5102092PMC
October 2016
5 Reads

Photoperiod Modulates Fast Delayed Rectifier Potassium Currents in the Mammalian Circadian Clock.

ASN Neuro 2016 10 3;8(5). Epub 2016 Oct 3.

Leiden University Medical Center, Leiden, The Netherlands.

One feature of the mammalian circadian clock, situated in the suprachiasmatic nucleus (SCN), is its ability to measure day length and thereby contribute to the seasonal adaptation of physiology and behavior. The timing signal from the SCN, namely the 24 hr pattern of electrical activity, is adjusted according to the photoperiod being broader in long days and narrower in short days. Vasoactive intestinal peptide and gamma-aminobutyric acid play a crucial role in intercellular communication within the SCN and contribute to the seasonal changes in phase distribution. Read More

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http://dx.doi.org/10.1177/1759091416670778DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5051630PMC
October 2016
13 Reads

Enhanced Histochemical Detection of Iron in Paraffin Sections of Mouse Central Nervous System Tissue: Application in the APP/PS1 Mouse Model of Alzheimer's Disease.

ASN Neuro 2016 Oct 28;8(5). Epub 2016 Sep 28.

Department of Molecular and Integrative Physiology, University of Kansas Medical Center, KS, USA

Histochemical methods of detecting iron in the rodent brain result mainly in the labeling of oligodendrocytes, but as all cells utilize iron, this observation suggests that much of the iron in the central nervous system goes undetected. Paraffin embedding of tissue is a standard procedure that is used to prepare sections for microscopic analysis. In the present study, we questioned whether we could modify the iron histochemical procedure to enable a greater detection of iron in paraffin sections. Read More

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http://dx.doi.org/10.1177/1759091416670978DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5043597PMC
October 2016
12 Reads

Transcriptional Fingerprint of Hypomyelination in Zfp191null and Shiverer (Mbpshi) Mice.

ASN Neuro 2016 Oct 28;8(5). Epub 2016 Sep 28.

Department of Neurology, The University of Chicago Center for Peripheral Neuropathy, The University of Chicago, IL, USA

The transcriptional program that controls oligodendrocyte maturation and central nervous system (CNS) myelination has not been fully characterized. In this study, we use high-throughput RNA sequencing to analyze how the loss of a key transcription factor, zinc finger protein 191 (ZFP191), results in oligodendrocyte development abnormalities and CNS hypomyelination. Using a previously described mutant mouse that is deficient in ZFP191 protein expression (Zfp191), we demonstrate that key transcripts are reduced in the whole brain as well as within oligodendrocyte lineage cells cultured in vitro To determine whether the loss of myelin seen in Zfp191 mice contributes indirectly to these perturbations, we also examined the transcriptome of a well-characterized mouse model of hypomyelination, in which the myelin structural protein myelin basic protein (MBP) is deficient. Read More

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http://dx.doi.org/10.1177/1759091416670749DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5046175PMC
October 2016
7 Reads

Intranasal Administration of Interferon Beta Attenuates Neuronal Apoptosis via the JAK1/STAT3/BCL-2 Pathway in a Rat Model of Neonatal Hypoxic-Ischemic Encephalopathy.

ASN Neuro 2016 Oct 28;8(5). Epub 2016 Sep 28.

Department of Physiology and Pharmacology, Loma Linda University School of Medicine, CA, USA

Neonatal hypoxic-ischemic encephalopathy (HIE) is an injury that often leads to detrimental neurological deficits. Currently, there are no established therapies for HIE and it is critical to develop treatments that provide protection after HIE. The objective of this study was to investigate the ability of interferon beta (IFNβ) to provide neuroprotection and reduce apoptosis after HIE. Read More

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http://dx.doi.org/10.1177/1759091416670492DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5043595PMC
October 2016
10 Reads

Anti-Sulfoglucuronosyl Paragloboside Antibody: A Potential Serologic Marker of Amyotrophic Lateral Sclerosis.

ASN Neuro 2016 Oct 28;8(5). Epub 2016 Sep 28.

Department of Neuroscience and Regenerative Medicine, Medical College of Georgia, Augusta University, GA, USA Department of Neurology, ALS Clinic, Medical College of Georgia, Augusta University, GA, USA

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by progressive degeneration of upper and lower motor neurons. Although the etiology of ALS is obscure, genetic studies of familiar ALS suggest a multifactorial etiology for this condition. Similarly, there probably are multiple causes for sporadic ALS. Read More

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http://dx.doi.org/10.1177/1759091416669619DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5043593PMC
October 2016
3 Reads

Clock Genes in Glia Cells: A Rhythmic History.

ASN Neuro 2016 Oct 25;8(5). Epub 2016 Sep 25.

Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, Ciudad de México, México

Circadian rhythms are periodic patterns in biological processes that allow the organisms to anticipate changes in the environment. These rhythms are driven by the suprachiasmatic nucleus (SCN), the master circadian clock in vertebrates. At a molecular level, circadian rhythms are regulated by the so-called clock genes, which oscillate in a periodic manner. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5037500PMC
http://dx.doi.org/10.1177/1759091416670766DOI Listing
October 2016
2 Reads