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[PMID]: 27151771
[Au] Autor:Chang Q; Martin LJ
[Ad] Address:Department of Pathology, Division of Neuropathology, Johns Hopkins University School of Medicine, MD 21205, United States. Electronic address: qchang1@jhmi.edu.
[Ti] Title:Voltage-gated calcium channels are abnormal in cultured spinal motoneurons in the G93A-SOD1 transgenic mouse model of ALS.
[So] Source:Neurobiol Dis;93:78-95, 2016 Sep.
[Is] ISSN:1095-953X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by progressive loss of motoneurons. Hyperexcitability and excitotoxicity have been implicated in the early pathogenesis of ALS. Studies addressing excitotoxic motoneuron death and intracellular Ca(2+) overload have mostly focused on Ca(2+) influx through AMPA glutamate receptors. However, intrinsic excitability of motoneurons through voltage-gated ion channels may also have a role in the neurodegeneration. In this study we examined the function and localization of voltage-gated Ca(2+) channels in cultured spinal cord motoneurons from mice expressing a mutant form of human superoxide dismutase-1 with a Gly93→Ala substitution (G93A-SOD1). Using whole-cell patch-clamp recordings, we showed that high voltage activated (HVA) Ca(2+) currents are increased in G93A-SOD1 motoneurons, but low voltage activated Ca(2+) currents are not affected. G93A-SOD1 motoneurons also have altered persistent Ca(2+) current mediated by L-type Ca(2+) channels. Quantitative single-cell RT-PCR revealed higher levels of Ca1a, Ca1b, Ca1c, and Ca1e subunit mRNA expression in G93A-SOD1 motoneurons, indicating that the increase of HVA Ca(2+) currents may result from upregulation of Ca(2+) channel mRNA expression in motoneurons. The localizations of the Ca1B N-type and Ca1D L-type Ca(2+) channels in motoneurons were examined by immunocytochemistry and confocal microscopy. G93A-SOD1 motoneurons had increased Ca1B channels on the plasma membrane of soma and dendrites. Ca1D channels are similar on the plasma membrane of soma and lower on the plasma membrane of dendrites of G93A-SOD1 motoneurons. Our study demonstrates that voltage-gated Ca(2+) channels have aberrant functions and localizations in ALS mouse motoneurons. The increased HVA Ca(2+) currents and PCCa current could contribute to early pathogenesis of ALS.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1607
[Cu] Class update date: 160702
[Lr] Last revision date:160702
[Js] Journal subset:IM
[St] Status:In-Data-Review

  2 / 201377 MEDLINE  
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[PMID]: 27097894
[Au] Autor:Mallipattu SK; He JC
[Ad] Address:Division of Nephrology, Department of Medicine, Stony Brook University, Stony Brook, New York;
[Ti] Title:The podocyte as a direct target for treatment of glomerular disease?
[So] Source:Am J Physiol Renal Physiol;311(1):F46-51, 2016 Jul 1.
[Is] ISSN:1522-1466
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The Centers for Disease Control and Prevention estimates more than 10% of adults in the United States, over 20 million Americans, have chronic kidney disease (CKD). A failure to maintain the glomerular filtration barrier directly contributes to the onset of CKD. The visceral epithelial cells, podocytes, are integral to the maintenance of this renal filtration barrier. Direct podocyte injury contributes to the onset and progression of glomerular diseases such as minimal change disease (MCD), focal segmental glomerular sclerosis (FSGS), diabetic nephropathy, and HIV-associated nephropathy (HIVAN). Since podocytes are terminally differentiated with minimal capacity to self-replicate, they are extremely sensitive to cellular injury. In the past two decades, our understanding of the mechanism(s) by which podocyte injury occurs has greatly expanded. With this newfound knowledge, therapeutic strategies have shifted to identifying targets directed specifically at the podocyte. Although the systemic effects of these agents are important, their direct effect on the podocyte proves to be essential in ameliorating glomerular disease. In this review, we highlight the mechanisms by which these agents directly target the podocyte independent of its systemic effects.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1607
[Cu] Class update date: 160702
[Lr] Last revision date:160702
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1152/ajprenal.00184.2016

  3 / 201377 MEDLINE  
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[PMID]: 26852120
[Au] Autor:Nostramo R; Herman PK
[Ad] Address:Department of Molecular Genetics, The Ohio State University, Columbus, OH, 43210, USA.
[Ti] Title:Deubiquitination and the regulation of stress granule assembly.
[So] Source:Curr Genet;62(3):503-6, 2016 Aug.
[Is] ISSN:1432-0983
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Stress granules (SGs) are evolutionarily conserved ribonucleoprotein (RNP) structures that form in response to a variety of environmental and cellular cues. The presence of these RNP granules has been linked to a number of human diseases, including neurodegenerative disorders like amyotrophic lateral sclerosis (ALS) and spinocerebellar ataxia type 2 (Li et al., J Cell Biol 201:361-372, 2013; Nonhoff et al., Mol Biol Cell 18:1385-1396, 2007). Understanding how the assembly of these granules is controlled could, therefore, suggest possible routes of therapy for patients afflicted with these conditions. Interestingly, several reports have identified a potential role for protein deubiquitination in the assembly of these RNP granules. In particular, recent work has found that a specific deubiquitinase enzyme, Ubp3, is required for efficient SG formation in S. cerevisiae (Nostramo et al., Mol Cell Biol 36:173-183, 2016). This same enzyme has been linked to SGs in other organisms, including humans and the fission yeast, Schizosaccharomyces pombe (Takahashi et al., Mol Cell Biol 33:815-829, 2013; Wang et al., RNA 18:694-703, 2012). At first glance, these observations suggest that a striking degree of conservation exists for a ubiquitin-based mechanism controlling SG assembly. However, the devil is truly in the details here, as the precise nature of the involvement of this deubiquitinating enzyme seems to vary in each organism. Here, we briefly review these differences and attempt to provide an overarching model for the role of ubiquitin in SG formation.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1607
[Cu] Class update date: 160702
[Lr] Last revision date:160702
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1007/s00294-016-0571-9

  4 / 201377 MEDLINE  
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[PMID]: 26950113
[Au] Autor:Jasiak-Zatonska M; Kalinowska-Lyszczarz A; Michalak S; Kozubski W
[Ad] Address:Department of Neurology, Poznan University of Medical Sciences, 49 Przybyszewskiego St., 60-355 Poznan, Poland. michalina.ja@gmail.com....
[Ti] Title:The Immunology of Neuromyelitis Optica-Current Knowledge, Clinical Implications, Controversies and Future Perspectives.
[So] Source:Int J Mol Sci;17(3):273, 2016.
[Is] ISSN:1422-0067
[Cp] Country of publication:Switzerland
[La] Language:eng
[Ab] Abstract:Neuromyelitis optica (NMO) is an autoimmune, demyelinating disorder of the central nervous system (CNS) with typical clinical manifestations of optic neuritis and acute transverse myelitis attacks. Previously believed to be a variant of multiple sclerosis (MS), it is now considered an independent disorder which needs to be differentiated from MS. The discovery of autoantibodies against aquaporin-4 (AQP4-IgGs) changed our understanding of NMO immunopathogenesis and revolutionized the diagnostic process. AQP4-IgG is currently regarded as a specific biomarker of NMO and NMO spectrum disorders (NMOsd) and a key factor in its pathogenesis. Nevertheless, AQP4-IgG seronegativity in 10%-25% of NMO patients suggests that there are several other factors involved in NMO immunopathogenesis, i.e., autoantibodies against aquaporin-1 (AQP1-Abs) and antibodies against myelin oligodendrocyte glycoprotein (MOG-IgGs). This manuscript reviews current knowledge about NMO immunopathogenesis, pointing out the controversial issues and showing potential directions for future research. Further efforts should be made to broaden our knowledge of NMO immunology which could have important implications for clinical practice, including the use of potential novel biomarkers to facilitate an early and accurate diagnosis, and modern treatment strategies improving long-term outcome of NMO patients.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Em] Entry month:1603
[Cu] Class update date: 160407
[Lr] Last revision date:160407
[Js] Journal subset:IM
[St] Status:In-Process

  5 / 201377 MEDLINE  
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[PMID]: 26826008
[Au] Autor:Hollinger KR; Alt J; Riehm AM; Slusher BS; Kaplin AI
[Ad] Address:Department of Psychiatry and Behavioral Sciences, Johns Hopkins University, Baltimore, MD 21287, USA; Department of Neurology, Johns Hopkins University, Baltimore, MD 21287, USA....
[Ti] Title:Dose-dependent inhibition of GCPII to prevent and treat cognitive impairment in the EAE model of multiple sclerosis.
[So] Source:Brain Res;1635:105-12, 2016 Mar 15.
[Is] ISSN:1872-6240
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:There are no treatments for cognitive impairment in multiple sclerosis (MS). Novel treatments can be evaluated in experimental autoimmune encephalomyelitis (EAE), a mouse model of MS that displays both physical and cognitive impairments. Inhibition of the neuropeptidase glutamate carboxypeptidase II (GCPII) has previously been shown to ameliorate cognitive impairment in EAE, but dosing has not yet been optimized and only a prevention treatment paradigm has been explored. In the study described herein, the dose response of the GCPII inhibitor 2-(phosphonomethyl)pentanedioic acid (2-PMPA) was evaluated for preventing cognitive impairment in EAE mice. Mice were immunized and received daily injections of vehicle or 2-PMPA (10, 30, 100, or 300 mg/kg) from the time of immunization (i.e. day 0). Although no doses of the drug altered physical disease severity, the 100mg/kg dose was most efficacious at preventing cognitive impairments in Barnes maze performance. Dose-related increases in brain NAAG levels were observed in post-mortem analysis, confirming target engagement. Using the 100mg/kg dose, we subsequently evaluated 2-PMPA׳s ability to treat EAE-induced symptoms by commencing treatment after the onset of physical signs of EAE (i.e. day 14). Mice were immunized for EAE and received daily injections of vehicle or 100mg/kg 2-PMPA starting two weeks post-immunization. Significant improvements in both cognitive performance and increases in brain NAAG levels were observed. GCPII inhibition is a promising treatment for cognitive impairment in MS, and doses providing equivalent exposures to 100mg/kg 2-PMPA in mice should be evaluated in clinical studies for the prevention and/or treatment of MS-related cognitive impairment.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Em] Entry month:1603
[Js] Journal subset:IM
[St] Status:In-Process

  6 / 201377 MEDLINE  
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[PMID]: 26663440
[Au] Autor:White MK; Sariyer IK; Gordon J; Delbue S; Pietropaolo V; Berger JR; Khalili K
[Ad] Address:Department of Neuroscience, Center for Neurovirology and Comprehensive NeuroAIDS Center, Lewis Katz School of Medicine at Temple University, Philadelphia, Pennsylvania, USA....
[Ti] Title:Diagnostic assays for polyomavirus JC and progressive multifocal leukoencephalopathy.
[So] Source:Rev Med Virol;26(2):102-14, 2016 Mar.
[Is] ISSN:1099-1654
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Progressive multifocal leukoencephalopathy (PML) is a devastating and often fatal demyelinating disease of the central nervous system for which effective therapies are lacking. It is caused by the replication of polyomavirus JC (JCV) in the oligodendrocytes and astrocytes leading to their cytolytic death and loss of myelin from the subcortical white matter. While the virus is very common in human populations worldwide, the incidence of the disease is very low and confined almost exclusively to individuals with some form of immunological dysfunction. However, the number of people who constitute the at-risk population is growing larger and includes individuals with HIV-1/AIDS and patients receiving immunomodulatory therapies such as multiple sclerosis patients treated with natalizumab. Further adding to the public health significance of this disease are the difficulties encountered in the diagnosis of PML and the lack of useful biomarkers for PML progression. In this review, we examine the diagnostic assays that are available for different aspects of the JCV life cycle, their usefulness and drawbacks, and the prospects for improvements.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; REVIEW
[Em] Entry month:1603
[Cu] Class update date: 160529
[Lr] Last revision date:160529
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1002/rmv.1866

  7 / 201377 MEDLINE  
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[PMID]: 26295502
[Au] Autor:McEwan L; Caon C; Chieffe C; Mayer L; Saldana-King T; Miller CE
[Ad] Address:London Health Sciences Centre, London, Ontario, Canada (Ms McEwan); Multiple Sclerosis Center, Wayne State University School of Medicine, Detroit, Michigan (Ms Caon); Neuroscience Center, Allegheny General Hospital, Pittsburgh, Pennsylvania (Ms Chieffe); Central Texas Neurology Consultants, Round Rock, Texas (Dr Mayer); Multiple Sclerosis Comprehensive Care Center, Baylor College of Medicine, Houston, Texas (Ms Saldana-King); Genzyme, Cambridge, Massachusetts (Dr Miller). Lynn McEwan, MScN, NP, MSCN, CNNc, is a nurse practitioner at the Multiple Sclerosis Clinic of the London Health Sciences Centre in London, Ontario, Canada. She has specialized in the care of patients with multiple sclerosis for 25 years and is certified in multiple sclerosis and neuroscience nursing. Ms. McEwan has published and lectured on a variety of multiple sclerosis-related topics from disease management to nursing. She is a past president of the Multiple Sclerosis Nursing International Certification Board. Christina Caon, MSN, RN, NP-C, is a nurse practitioner and the assistant director of clinical research at the Multiple Sclerosis Center at Wayne State University. She has been involved with clinical trial research and numerous investigator-initiated trials for more than 14 years. She also has been an invited speaker and presented data at numerous national and international meetings focused on multiple sclerosis. Carol Chieffe, MSCN, RN, CCRC, is a clinical nurse at Allegheny General Hospital's Multiple Sclerosis Treatment Center, where she was instrumental in the development of the infusion center. She is active with the National Multiple Sclerosis Society as a health care advocate for government affairs on the state and federal levels. Lori Mayer, DNP, MSN, RN, the director of medical research services for the Multiple Sclerosis Clinic of Central Texas, manages multiple sclerosis clinical research programs, patient-centered education, and clinical care. In addition, she writes posters an
[Ti] Title:Best Practices in Alemtuzumab Administration: Practical Recommendations for Infusion in Patients With Multiple Sclerosis.
[So] Source:J Infus Nurs;39(2):93-104, 2016 Mar-Apr.
[Is] ISSN:1539-0667
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:With the growing complexity of multiple sclerosis (MS) care, nursing professionals have increasing responsibility in managing clinical disease and treatment. Nursing professionals and other health care providers play important roles in educating patients about disease-modifying therapy options, the course of therapy, and managing potential adverse effects. A panel of nursing and MS experts was convened and used a modified Delphi method to reach consensus on best-practice recommendations for alemtuzumab infusion in MS patients. This valuable clinical resource provides a practical guide for clinicians to optimize patient education and implement strategies for infusion-associated reaction prophylaxis and management when administering alemtuzumab.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1603
[Js] Journal subset:N
[St] Status:In-Process
[do] DOI:10.1097/NAN.0000000000000127

  8 / 201377 MEDLINE  
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[PMID]: 26765264
[Au] Autor:Berge T; Leikfoss IS; Brorson IS; Bos SD; Page CM; Gustavsen MW; Bjølgerud A; Holmøy T; Celius EG; Damoiseaux J; Smolders J; Harbo HF; Spurkland A
[Ad] Address:Department of Neurology, Oslo University Hospital, Oslo, Norway....
[Ti] Title:The multiple sclerosis susceptibility genes TAGAP and IL2RA are regulated by vitamin D in CD4+ T cells.
[So] Source:Genes Immun;17(2):118-27, 2016 Mar.
[Is] ISSN:1476-5470
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Multiple sclerosis (MS) is an inflammatory, demyelinating disorder of the central nervous system that develops in genetically susceptible individuals. The majority of the MS-associated gene variants are located in genetic regions with importance for T-cell differentiation. Vitamin D is a potent immunomodulator, and vitamin D deficiency has been suggested to be associated with increased MS disease susceptibility and activity. In CD4+ T cells, we have analyzed in vitro vitamin D responsiveness of genes that contain an MS-associated single-nucleotide polymorphism (SNP) and with one or more vitamin D response elements in their regulatory regions. We identify IL2RA and TAGAP as novel vitamin D target genes. The vitamin D response is observed in samples from both MS patients and controls, and is not dependent on the genotype of MS-associated SNPs in the respective genes.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1603
[Cu] Class update date: 160317
[Lr] Last revision date:160317
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1038/gene.2015.61

  9 / 201377 MEDLINE  
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[PMID]: 26190642
[Au] Autor:Török N; Török R; Klivényi P; Engelhardt J; Vécsei L
[Ad] Address:Department of Neurology, Faculty of Medicine, Albert Szent-Györgyi Clinical Centre, University of Szeged, Szeged, Hungary....
[Ti] Title:Investigation of vitamin D receptor polymorphisms in amyotrophic lateral sclerosis.
[So] Source:Acta Neurol Scand;133(4):302-8, 2016 Apr.
[Is] ISSN:1600-0404
[Cp] Country of publication:Denmark
[La] Language:eng
[Ab] Abstract:BACKGROUND: Amyotrophic lateral sclerosis (ALS) patients manifest aberrations in the vitamin D endocrine system, with a vitamin D deficiency. Genetic investigations have identified those proteins which link vitamin D to ALS pathology: major histocompatibility complex class II molecules, toll-like receptors, poly(ADP ribose) polymerase-1, haeme oxygenase-1, the reduced form of nicotinamide adenine dinucleotide phosphate and calcium-binding proteins. Vitamin D additionally impacts ALS through cell-signalling mechanisms: glutamate, matrix metalloproteinases, the Wnt/ß-catenin signalling pathway, mitogen-activated protein kinase pathways, prostaglandins, reactive oxygen species and nitric oxide synthase, but its role has been only poorly investigated. OBJECTIVE: Our aim was to investigate vitamin D receptor (VDR) gene single nucleotide polymorphisms (SNPs) in an ALS population. This gene encodes the nuclear hormone receptor for vitamin D3. MATERIALS AND METHODS: A total of 75 consecutive sporadic ALS patients (~20% of the Hungarian ALS population) and 97 healthy controls were enrolled to investigate the possible effects of the different VDR alleles. A restriction fragment length polymorphism technique was utilized for allele discrimination. RESULTS: One of the four investigated SNPs was associated with the disease, but none of the alleles of these SNPs influenced the age at disease onset. The ApaI A allele was more frequent in the ALS group than in the control group and may be an ALS risk factor. CONCLUSIONS: This is the first verification of the genetic link between ALS and VDR. However, further studies are needed to confirm these findings.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1603
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1111/ane.12463

  10 / 201377 MEDLINE  
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[PMID]: 26079721
[Au] Autor:Deretzi G; Gavalas E; Boziki M; Tsiptsios D; Polyzos SA; Venizelos I; Zavos C; Koutlas E; Tsiptsios I; Katsinelos P; Kountouras J
[Ad] Address:Multiple Sclerosis Unit, Department of Neurology, "Papageorgiou" Hospital, Thessaloniki, Greece....
[Ti] Title:Impact of Helicobacter pylori on multiple sclerosis-related clinically isolated syndrome.
[So] Source:Acta Neurol Scand;133(4):268-75, 2016 Apr.
[Is] ISSN:1600-0404
[Cp] Country of publication:Denmark
[La] Language:eng
[Ab] Abstract:OBJECTIVES: There are no data regarding the relationship between Helicobacter pylori infection (Hp-I) and clinically isolated syndrome (CIS) suggestive of multiple sclerosis. The purpose of this pilot study was to investigate the association between active Hp-I, confirmed by histology, and CIS and to evaluate the impact of Hp eradication on the CIS clinical course. MATERIAL AND METHODS: We conducted a study on 48 patients with CIS and 20 matched controls. At baseline, apart from histology, serum anti-Hp-specific IgG titer, inflammatory mediators, and HLA-A, HLA-B, HLA-DR genetic polymorphisms were estimated. Hp-positive patients received standard triple eradication regimen, and all patients were followed up for 2 years. RESULTS: The prevalence of Hp-I was significantly higher in patients with CIS (43/48, 89.6%) than in control (10/20, 50%) (P < 0.001, OR: 8.6, 95% CI: 2.4-30.8). When compared with controls, patients with CIS also showed significantly higher serum anti-Hp IgG titer and HLA-A26, HLA-A30, and HLA-B57 frequencies. Hp-positive patients also showed higher serum concentrations of inflammatory cytokines and homocysteine. At 2-year clinical endpoint, in the subgroup of CIS patients with successful Hp eradication, the number of patients who presented with a second episode was significantly lower accompanied by significant improvement in mean Expanded Disability Status Scale score. CONCLUSIONS: Hp-I seems more frequent in a Greek CIS cohort and its eradication might delay CIS progression, suggesting a possible link between Hp-I and CIS.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1603
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1111/ane.12453


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