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[PMID]: 25372080
[Au] Autor:Buzhor E; Leshansky L; Blumenthal J; Barash H; Warshawsky D; Mazor Y; Shtrichman R
[Ad] Address:LifeMap Sciences Ltd, Tel Aviv, Israel.
[Ti] Title:Cell-based therapy approaches: the hope for incurable diseases.
[So] Source:Regen Med;9(5):649-72, 2014 Sep.
[Is] ISSN:1746-076X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Cell therapies aim to repair the mechanisms underlying disease initiation and progression, achieved through trophic effect or by cell replacement. Multiple cell types can be utilized in such therapies, including stem, progenitor or primary cells. This review covers the current state of cell therapies designed for the prominent disorders, including cardiovascular, neurological (Parkinson's disease, amyotrophic lateral sclerosis, stroke, spinal cord injury), autoimmune (Type 1 diabetes, multiple sclerosis, Crohn's disease), ophthalmologic, renal, liver and skeletal (osteoarthritis) diseases. Various cell therapies have reached advanced clinical trial phases with potential marketing approvals in the near future, many of which are based on mesenchymal stem cells. Advances in pluripotent stem cell research hold great promise for regenerative medicine. The information presented in this review is based on the analysis of the cell therapy collection detailed in LifeMap Discovery(®) (LifeMap Sciences Inc., USA) the database of embryonic development, stem cell research and regenerative medicine.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1411
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.2217/rme.14.35

  2 / 179533 MEDLINE  
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[PMID]: 25372079
[Au] Autor:Allers C; Jones JA; Lasala GP; Minguell JJ
[Ad] Address:TCA Cellular Therapy, LLC, 101 Judge Tanner Blvd, Suite 502, Covington, LA 70433, USA.
[Ti] Title:Mesenchymal stem cell therapy for the treatment of amyotrophic lateral sclerosis: signals for hope?
[So] Source:Regen Med;9(5):637-47, 2014 Sep.
[Is] ISSN:1746-076X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Based on the distinctive cellular, molecular and immunomodulatory traits of mesenchymal stem cells (MSC), it has been postulated that these cells may play a critical role in regenerative medicine. In addition to the participation of MSC in the repair of mesodermal-derived tissues (bone, cartilage), robust data have suggested that MSC may also play a reparative role in conditions involving damage of cells of ectodermal origin. The above content has been supported by the capability of MSC to differentiate into neuron-like cells as well as by a competence to generate a 'neuroprotective' environment. In turn, several preclinical studies have put forward the concept that MSC therapy may represent an option for the treatment of several neurological disorders and injuries, including amyotrophic lateral sclerosis. We expect that the above foundations, which have inspired this review, may result in the founding of an effective and/or palliative therapy for amyotrophic lateral sclerosis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1411
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.2217/rme.14.30

  3 / 179533 MEDLINE  
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[PMID]: 25372031
[Au] Autor:Padhi AK; Banerjee K; Gomes J; Banerjee M
[Ad] Address:Kusuma School of Biological Sciences, Indian Institute of Technology Delhi, New Delhi, India....
[Ti] Title:Computational and functional characterization of angiogenin mutations, and correlation with amyotrophic lateral sclerosis.
[So] Source:PLoS One;9(11):e111963, 2014.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The Angiogenin (ANG) gene is frequently mutated in patients suffering from the neurodegenerative disease - amyotrophic lateral sclerosis (ALS). Most of the ALS-causing mutations in Angiogenin affect either its ribonucleolytic or nuclear translocation activity. Here we report the functional characterization of two previously uncharacterized missense mutations in Angiogenin - D22G and L35P. We predict the nature of loss-of-function(s) in these mutants through our previously established Molecular Dynamics (MD) simulation extended to 100 ns, and show that the predictions are entirely validated through biochemical studies with wild-type and mutated proteins. Based on our studies, we provide a biological explanation for the loss-of-function of D22G-Angiogenin leading to ALS, and suggest that the L35P-Angiogenin mutation would probably cause ALS symptoms in individuals harboring this mutation. Our study thus highlights the strength of MD simulation-based predictions, and suggests that this method can be used for correlating mutations in Angiogenin or other effector proteins with ALS symptoms.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1411
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1371/journal.pone.0111963

  4 / 179533 MEDLINE  
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[PMID]: 25374348
[Au] Autor:Rademakers R; van Blitterswijk M
[Ad] Address:Department of Neuroscience, Mayo Clinic, Jacksonville, FL 32224, USA. Electronic address: rademakers.rosa@mayo.edu.
[Ti] Title:Excess of Rare Damaging TUBA4A Variants Suggests Cytoskeletal Defects in ALS.
[So] Source:Neuron;84(2):241-3, 2014 Oct 22.
[Is] ISSN:1097-4199
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Identifying disease genes implicated in late-onset neurodegenerative disorders can be challenging due to the lack of DNA samples from multiple affected family members. To overcome this limitation, Smith et al. (2014) report in this issue of Neuron the first exome-wide rare variant analysis in unrelated familial amyotrophic lateral sclerosis (ALS) patients associating TUBA4A with ALS.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1411
[Js] Journal subset:IM
[St] Status:In-Data-Review

  5 / 179533 MEDLINE  
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[PMID]: 25374694
[Au] Autor:Duffy SS; Lees JG; Moalem-Taylor G
[Ad] Address:School of Medical Science, The University of New South Wales, Wallace Wurth Building East, Level 3, Room 327, Sydney, NSW 2052, Australia.
[Ti] Title:The contribution of immune and glial cell types in experimental autoimmune encephalomyelitis and multiple sclerosis.
[So] Source:Mult Scler Int;2014:285245, 2014.
[Is] ISSN:2090-2654
[Cp] Country of publication:Egypt
[La] Language:eng
[Ab] Abstract:Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system characterised by widespread areas of focal demyelination. Its aetiology and pathogenesis remain unclear despite substantial insights gained through studies of animal models, most notably experimental autoimmune encephalomyelitis (EAE). MS is widely believed to be immune-mediated and pathologically attributable to myelin-specific autoreactive CD4+ T cells. In recent years, MS research has expanded beyond its focus on CD4+ T cells to recognise the contributions of multiple immune and glial cell types to the development, progression, and amelioration of the disease. This review summarises evidence of T and B lymphocyte, natural killer cell, macrophage/microglial, astrocytic, and oligodendroglial involvement in both EAE and MS and the intercommunication and influence of each cell subset in the inflammatory process. Despite important advances in the understanding of the involvement of these cell types in MS, many questions still remain regarding the various subsets within each cell population and their exact contribution to different stages of the disease.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1411
[Da] Date of entry for processing:141106
[St] Status:PubMed-not-MEDLINE
[do] DOI:10.1155/2014/285245

  6 / 179533 MEDLINE  
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[PMID]: 25178511
[Au] Autor:Marrali G; Casale F; Salamone P; Fuda G; Caorsi C; Amoroso A; Brunetti M; Restagno G; Barberis M; Bertuzzo D; Canosa A; Moglia C; Calvo A; Chiò A
[Ad] Address:"Rita Levi Montalcini" Department of Neuroscience, ALS Centre, University of Torino, Via Cherasco 15, 10126, Turin, Italy, giuseppemarrali@hotmail.it.
[Ti] Title:NADPH oxidase (NOX2) activity is a modifier of survival in ALS.
[So] Source:J Neurol;261(11):2178-83, 2014 Nov.
[Is] ISSN:1432-1459
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:NADPH-oxidases (NOX) catalyze the formation of reactive oxygen species (ROS), which play a role in the development of neurological diseases, particularly those generated by the phagocytic isoform NOX2. Increased ROS has been observed in the amyotrophic lateral sclerosis (ALS) SOD1 transgenic mouse, and in this preclinical model the inactivation of NOX2 decreases ROS production and extends survival. Our aim was to evaluate NOX2 activity measuring neutrophil oxidative burst in a cohort of 83 ALS patients, and age- and gender-matched healthy controls. Oxidative burst was measured directly in fresh blood using Phagoburstâ„¢ assay by flow cytometry. Mean fluorescence intensity (MFI), emitted in response to different stimuli, leads to produce ROS and corresponds to the percentage of oxidizing cells and their enzymatic activity (GeoMean). No difference was found between the MFI values in cases and controls. NOX2 activity was independent from gender and age, and in patients was not related to disease duration, site of onset (bulbar vs. spinal), or ALSFRS-R score. However, patients with a NOX2 activity lower than the median value showed a 1-year increase of survival from onset (p = 0.011). The effect of NOX2 was independent from other known prognostic factors. These findings are in keeping with the observations in the mouse model of ALS, and demonstrate the strong role of NOX2 in modifying progression in ALS patients. A proper modulation of NOX2 activity might hold therapeutic potential for ALS.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1411
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1007/s00415-014-7470-0

  7 / 179533 MEDLINE  
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[PMID]: 25119836
[Au] Autor:Ziemssen T; Bajenaru OA; Carrá A; de Klippel N; de Sá JC; Edland A; Frederiksen JL; Heinzlef O; Karageorgiou KE; Lander Delgado RH; Landtblom AM; Macías Islas MA; Tubridy N; Gilgun-Sherki Y
[Ad] Address:Neurologische Universitätsklinik, Klinikum Carl Gustav Carus, Fetscherstraße 74, 01307, Dresden, Germany, Tjalf.Ziemssen@uniklinikum-dresden.de.
[Ti] Title:A 2-year observational study of patients with relapsing-remitting multiple sclerosis converting to glatiramer acetate from other disease-modifying therapies: the COPTIMIZE trial.
[So] Source:J Neurol;261(11):2101-11, 2014 Nov.
[Is] ISSN:1432-1459
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:Studies suggest that patients with relapsing-remitting multiple sclerosis (RRMS) who do not benefit from other disease-modifying treatments (DMTs) may benefit from converting to glatiramer acetate (GA). COPTIMIZE was a 24-month observational study designed to assess the disease course of patients converting to GA 20 mg daily from another DMT. Eligible patients had converted to GA and had received prior DMT for 3-6 months, depending on the reasons for conversion. Patients were assessed at baseline and at 6, 12, 18, and 24 months. In total, 672 patients from 148 centers worldwide were included in the analysis. Change of therapy to GA was prompted primarily by lack of efficacy (53.6 %) or intolerable adverse events (AEs; 44.8 %). Over a 24-month period, 72.7 % of patients were relapse free. Mean annual relapse rate decreased from 0.86 [95 % confidence interval (CI) 0.81-0.91] before the change to 0.32 (95 % CI 0.26-0.40; p < 0.0001) at last observation, while the progression of disability was halted, as the Kurtzke Expanded Disability Status Scale (EDSS) scores remained stable. Patients improved significantly (p < 0.05) on measures of fatigue, quality of life, depression, and cognition; mobility scores remained stable. The results indicate that changing RRMS patients to GA is associated with positive treatment outcomes.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1411
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1007/s00415-014-7446-0

  8 / 179533 MEDLINE  
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[PMID]: 25373461
[Au] Autor:Doi Y; Atsuta N; Sobue G; Morita M; Nakano I
[Ad] Address:Area on Epidemiological Research, National Institute of Public Health.
[Ti] Title:Prevalence and incidence of amyotrophic lateral sclerosis in Japan.
[So] Source:J Epidemiol;24(6):494-9, 2014 Nov 5.
[Is] ISSN:1349-9092
[Cp] Country of publication:Japan
[La] Language:eng
[Ab] Abstract:BACKGROUND: Previous studies have reported a high incidence of amyotrophic lateral sclerosis (ALS) in endemic foci in the Kii Peninsula, Japan. However, little is known about the ALS frequency in the whole country. Furthermore, the presence of ethnic variation in the incidence of ALS remains unknown. METHODS: We conducted a nationwide survey of ALS frequency in 2013 to estimate its annual prevalence and incidence. ALS was diagnosed based on the El Escorial Criteria. The study period was the 2009 fiscal year, from April 2009 to March 2010. To compare the incidence of ALS among prefectures, standardized incidence ratios (SIRs) and 95% confidence intervals (CIs) were calculated under the assumption of Poisson distribution. RESULTS: The annual crude prevalence and incidence rates per 100 000 people per year were 9.9 (95% CI 9.7-10.1) and 2.2 (95% CI 2.1-2.3), respectively. The age group with the highest prevalence as well as incidence was 70-79 years, and the male-female ratio was approximately 1.5. The annual incidence rate adjusted for age and sex using the 2000 U.S. standard population was 2.3 (95% CI 2.2-2.4) per 100 000 people. Some prefectures had significantly high SIRs: Okinawa, Nara and Wakayama in the Kii Peninsula, and Niigata for males; Kumamoto for females. CONCLUSIONS: This is the first report on the annual prevalence and incidence of ALS in the representative population of Japan. We identified some prefectures with a high incidence of ALS. However, the incidence of ALS in the Japanese population was much lower than in the Caucasian populations of Europe and North America.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1411
[Js] Journal subset:IM
[St] Status:In-Data-Review

  9 / 179533 MEDLINE  
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[PMID]: 25373133
[Au] Autor:Moses H
[Ti] Title:Recognizing and overcoming potential barriers to oral medications for MS.
[So] Source:J Clin Psychiatry;75(10):e28, 2014 Oct.
[Is] ISSN:1555-2101
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Three FDA-approved oral medications are available for the treatment of relapsing forms of multiple sclerosis: fingolimod, teriflunomide, and dimethyl fumarate. While injection and IV treatments have proven to be beneficial, these newer oral agents also offer positive outcomes for patients. Numerous barriers exist, though, for these oral agents, including the unknown long-term efficacy and safety and potential side effects. Despite possible side effects, oral agents provide convenience, ease of use, and the elimination of injection/IV administration-site pain. To ensure MS patients receive the most appropriate individualized care, clinicians should present all of the available treatment options to both newly diagnosed and established patients.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1411
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.4088/JCP.13037nr3c

  10 / 179533 MEDLINE  
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[PMID]: 24547735
[Au] Autor:Liu M; Hu X; Wang Y; Chen X; Wu J
[Ad] Address:1Department of Neurology, The Third Affiliated Hospital of Soochow University, Changzhou, China.
[Ti] Title:Association of IL-23 and its receptor gene single-nucleotide polymorphisms with multiple sclerosis in Chinese southern population.
[So] Source:Int J Neurosci;124(12):904-7, 2014 Dec.
[Is] ISSN:1563-5279
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:The subunit of IL-23 (IL12B) and its receptor (IL23R) gene single-nucleotide polymorphisms (SNPs) have been shown to be associated with several autoimmune diseases such as inflammatory bowel disease, psoriasis and ankylosing spondylitis. However, the association studies between multiple sclerosis (MS) and SNPs of IL12B or IL23R gene have been reported with inconsistent results in Caucasian population. These discrepancies prompted us to investigate whether IL12B and IL23R variants are associated with susceptibility to MS in Chinese southern population. In this study, we investigated four SNPs (rs2201841, rs10889677, rs7517847 in IL23R and rs3212227 in IL12B) in 178 MS patients and 221 health controls in southern China using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. There was no difference of genotype or allele distribution of these SNPs between MS patients and controls. No association was found between gene polymorphisms and clinical characteristics in MS patients. Furthermore, haplotypes analysis showed similar distribution of haplotype frequencies in MS patients and controls. Our study showed that the IL12B and IL23R gene SNPs does not seem to be associated with MS susceptibility in Chinese southern population.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1411
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.3109/00207454.2014.894044


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