Journal of Neuroimmunology (J NEUROIMMUNOL)

Publisher: International Society for Neuroimmunology, Elsevier

Journal description

The Journal of Neuroimmunology affords a forum for the publication of works applying immunologic methodology to the furtherance of the neurological sciences. Studies on all branches of the neurosciences, particularly fundamental and applied neurobiology, neurology, neuropathology, neurochemistry, neurovirology, neuroendocrinology, neuromuscular research, neuropharmacology and psychology, which involve either immunologic methodology (e.g. immunocytochemistry) or fundamental immunology (e.g. antibody and lymphocyte assays), are considered for publication. Works pertaining to multiple sclerosis, AIDS, amyotrophic lateral sclerosis, Guillain Barré Syndrome, myasthenia gravis, and brain tumors form a major focus. The scope of the Journal is broad, covering both research and clinical problems of neuroscientific interest.A major aim of the Journal is to encourage the development of immunologic approaches to analyse in further depth the interactions and specific properties of nervous tissue elements during development and disease.

Current impact factor: 2.79

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 Impact Factor 2.786
2012 Impact Factor 3.033
2011 Impact Factor 2.959
2010 Impact Factor 2.901
2009 Impact Factor 2.841
2008 Impact Factor 3.159
2007 Impact Factor 2.92
2006 Impact Factor 2.88
2005 Impact Factor 2.824
2004 Impact Factor 2.704
2003 Impact Factor 3.054
2002 Impact Factor 3.577
2001 Impact Factor 3.342
2000 Impact Factor 3.355
1999 Impact Factor 3.233
1998 Impact Factor 3.285
1997 Impact Factor 2.845
1996 Impact Factor 3.083
1995 Impact Factor 3.639
1994 Impact Factor 3.188
1993 Impact Factor 2.955
1992 Impact Factor 2.964

Impact factor over time

Impact factor
Year

Additional details

5-year impact 3.01
Cited half-life 7.80
Immediacy index 0.51
Eigenfactor 0.02
Article influence 0.86
Website Journal of Neuroimmunology website
Other titles Journal of neuroimmunology
ISSN 0165-5728
OCLC 7629351
Material type Periodical, Internet resource
Document type Journal / Magazine / Newspaper, Internet Resource

Publisher details

Elsevier

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Pre-print allowed on any website or open access repository
    • Voluntary deposit by author of authors post-print allowed on authors' personal website, arXiv.org or institutions open scholarly website including Institutional Repository, without embargo, where there is not a policy or mandate
    • Deposit due to Funding Body, Institutional and Governmental policy or mandate only allowed where separate agreement between repository and the publisher exists.
    • Permitted deposit due to Funding Body, Institutional and Governmental policy or mandate, may be required to comply with embargo periods of 12 months to 48 months .
    • Set statement to accompany deposit
    • Published source must be acknowledged
    • Must link to journal home page or articles' DOI
    • Publisher's version/PDF cannot be used
    • Articles in some journals can be made Open Access on payment of additional charge
    • NIH Authors articles will be submitted to PubMed Central after 12 months
    • Publisher last contacted on 18/10/2013
  • Classification
    ​ green

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Contactin-associated protein-like 2 (CASPR2) is one of the target antigens of voltage-gated potassium channels (VGKC) complex antibodies. There has been relatively little information in the literature regarding CASPR2 autoimmunity, especially in Asian population. We investigated the presence of CASPR2 antibodies in patients with presumed autoimmune neurological disorders and described the clinical features, laboratory findings, and responses to immunotherapy. Five patients were identified to be positive for CASPR2 antibodies. The results obtained here suggested that CASPR2 antibodies might be the possible cause of epilepsy even in the absence of typical features of limbic encephalitis and that immunotherapy could provide a favorable outcome. Copyright © 2015 Elsevier B.V. All rights reserved.
    Journal of Neuroimmunology 04/2015; 281. DOI:10.1016/j.jneuroim.2015.03.005
  • Journal of Neuroimmunology 03/2015; 280:56-7. DOI:10.1016/j.jneuroim.2015.02.003
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    ABSTRACT: Metabolomics has recently become a new technology using mass spectrometry (MS) and high-resolution proton nuclear magnetic resonance (NMR) to access metabolite profiles in biofluids or tissue extracts for the detection of biomarker molecules and biochemical effects induced by a disease or its therapeutic intervention. This review outlines recent advances in the use of metabolomic techniques to study autoimmune diseases (ADs), including multiple sclerosis (MS), rheumatoid arthritis (RA), inflammatory bowel diseases (IBD), autoimmune diabetes et al. Many studies have demonstrated that AD patients including subtypes of some diseases, and healthy individuals can be distinguished using metabolic profiling accompanied with well-established data analysis tools including principal component analysis (PCA) and partial least squares (PLS). These metabolites not only affect glucose, amino acid and lipid metabolism, but also involve alteration of neurotransmitters, nucleotides, immune responses and anti-inflammatory responses. Knowledge of unique metabolomic fingerprint in ADs could be useful for diagnosis, treatment, and detection mechanisms of diseases.
    Journal of Neuroimmunology 02/2015; 279. DOI:10.1016/j.jneuroim.2015.01.001
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    ABSTRACT: Vitamin D deficiency is associated with increased susceptibility to multiple sclerosis (MS) and increased disease activity. Vitamin D is a potent immunomodulator but the effects of vitamin D treatment on T cell memory have not been explored. We studied the effects of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) on T cell memory in MS patients (n = 10) and healthy controls (n = 10). In vitro treatment of PBMC cultures with 1,25(OH)2D3, led to a decrease in the proportion of effector memory T cells with an increase in naïve T cells, compared to vehicle in both groups. Further studies to unravel the mechanism of this effect and to understand its long-term implications are required.
    Journal of Neuroimmunology 02/2015; 279. DOI:10.1016/j.jneuroim.2014.12.018
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    ABSTRACT: The CXC chemokines (CXC-motif ligand 12 and CXC-motif ligand 14) and platelet-derived growth factor are suggested to modulate remyelination in the course of many demyelinating diseases. The present study compared the difference in the brain levels of these chemokines between patients with idiopathic demyelinating optic neuritis (IDON) and neuromyelitis optica (NMO) by measuring their concentrations in the cerebrospinal fluid using an enzyme linked immunosorbent assay. Our data indicate that the prognosis of neuritis depends on the remyelinating process that is impaired due to decreased chemokines. The much lower levels of chemokines would specifically indicate the severe neuritis, such as NMO. Copyright © 2014 Elsevier B.V. All rights reserved.
    Journal of Neuroimmunology 02/2015; 279:1-6. DOI:10.1016/j.jneuroim.2014.12.004
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    ABSTRACT: Rett syndrome is a neurodevelopmental disorder, which occurs in about 1:15,000 females and presents with neurologic and communication defects. It is transmitted as an X-linked dominant linked to mutations of the methyl-CpG-binding protein (MeCP2), a gene transcription suppressor, but its definitive pathogenesis is unknown thus hindering development of effective treatments. Almost half of children with Rett syndrome also have behavioral symptoms consistent with those of autism spectrum disorders (ASDs). PubMed was searched (2005-2014) using the terms: allergy, atopy, brain, brain-derived neurotrophic factor (BDNF), corticotropin-releasing hormone (CRH), cytokines, gene mutations, inflammation, mast cells (MCs), microglia, mitochondria, neurotensin (NT), neurotrophins, seizures, stress, and treatment. There are a number of intriguing differences and similarities between Rett syndrome and ASDs. Rett syndrome occurs in females, while ASDs more often in males, and the former has neurologic disabilities unlike ASDs. There is evidence of dysregulated immune system early in life in both conditions. Lack of microglial phagocytosis and decreased levels of BDNF appear to distinguish Rett syndrome from ASDs, in which there is instead microglia activation and/or proliferation and possibly defective BDNF signaling. Moreover, brain mast cell (MC) activation and focal inflammation may be more prominent in ASDs than Rett syndrome. The flavonoid luteolin blocks microglia and MC activation, provides BDNF-like activity, reverses Rett phenotype in mouse models, and has a significant benefit in children with ASDs. Appropriate formulations of luteolin or other natural molecules may be useful in the treatment of Rett syndrome. Copyright © 2014 Elsevier B.V. All rights reserved.
    Journal of Neuroimmunology 02/2015; 279C:33-38. DOI:10.1016/j.jneuroim.2014.12.003
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    ABSTRACT: Matrix metalloproteinase 9 (MMP9) plays an important role in the pathogenesis of multiple sclerosis (MS). However, the impact of genetic variants affecting MMP9 on MS susceptibility is still in debate.
    Journal of Neuroimmunology 01/2015; 279. DOI:10.1016/j.jneuroim.2015.01.008
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    ABSTRACT: Data regarding vitamin D in multiple sclerosis (MS) in Asia are limited. We investigated whether Japanese MS patients show decreased serum 25-hydroxyvitamin D [25(OH)D], 1,25-dihydroxyvitamin D [1,25(OH)2D], and vitamin D-binding protein (DBP) during winter. Mean serum 25(OH)D and 1,25(OH)2D levels were significantly lower in MS patients than in controls. There were no significant differences in serum 25(OH)D, 1,25(OH)2D, and DBP levels between patients or between controls from northern Japan (Hokkaido) and southern Japan (Kyushu). Serum vitamin D levels were low in Japanese MS patients but did not differ in patients from northern and southern Japan.
    Journal of Neuroimmunology 01/2015; 279. DOI:10.1016/j.jneuroim.2015.01.007
  • [Show abstract] [Hide abstract]
    ABSTRACT: Deficiency of vitamin D is an environmental risk factor for MS. Vitamin D has immunomodulatory effects, including promotion of T-cell differentiation into T-regulatory cells, which produces regulatory cytokines including TGF-β. Increasing serum vitamin D levels have been associated with decreased disease activity in MS patients, but there are only few studies concerning the immunological effects of vitamin D supplementation in MS. In this study we investigated the effect of weekly supplementation of vitamin D3 or placebo on serum levels of multiple cytokines in patients with relapsing remitting MS. The study was conducted on the patient cohort of the Finnish Vitamin D study. All patients were using IFN-beta-1b and were randomized to add-on treatment with either cholecalciferol 20,000IU/week or placebo. Concentrations of LAP (TGF-β), INF-γ, IL-17A, IL-2, IL-10, IL-9, IL-22, IL-6, IL-13, IL-4, IL-5, IL-1β and TNF-α were determined at screening and at 12months using commercial fluorescent bead immunoassay kits. LAP (TGF-β) levels increased significantly in the vitamin D treated group from a mean of 47 (SE 11) pg/ml to 55 (SE 14) pg/ml in 12months (p-value=0.0249). Placebo treatment had no significant effect on LAP levels. The levels of the other cytokines did not change significantly in either group. We showed increased serum latency activated peptide (LAP) of TGF-β levels in MS patients treated with vitamin D3. The immune regulatory effects of TGF-beta may play a role in the improved MRI outcomes that we observed earlier in the vitamin D treated group of patients. Copyright © 2015 Elsevier B.V. All rights reserved.
    Journal of Neuroimmunology 01/2015; 280. DOI:10.1016/j.jneuroim.2015.01.005
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    ABSTRACT: Inflammation in the meninges, tissues surrounding the brain and spinal cord that enclose the cerebrospinal fluid, closely parallels clinical exacerbations in relapsing-remitting experimental autoimmune encephalomyelitis (EAE). In preclinical disease, an influx of innate immune cells precedes loss of blood brain barrier (BBB) integrity and large-scale inflammation in the central nervous system (CNS). T cell infiltration into the meninges is observed in acute disease as well as during relapse, when neither BBB permeability nor significant increases in peripherally-derived immune cell numbers in the CNS are observed. These findings support the idea that the meninges are a gateway for immune cell access into the CNS, a finding that has important therapeutic implications. Copyright © 2014 Elsevier B.V. All rights reserved.
    Journal of Neuroimmunology 01/2015; 278C:112-122. DOI:10.1016/j.jneuroim.2014.12.009
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    ABSTRACT: Peripheral circulating cytokines are involved in immune to brain communication and systemic inflammation is considered a risk factor for flaring up the symptoms in most neurodegenerative diseases. We induced both central inflammatory demyelinating lesion, and systemic inflammation with an interleukin-1β expressing adenovector. The peripheral pro-inflammatory stimulus aggravated the ongoing central lesion independently of the blood-brain barrier (BBB) integrity. This model allows studying the role of specific molecules and cells (neutrophils) from the innate immune system, in the relationship between central and peripheral communication, and on relapsing episodes of demyelinating lesions, along with the role of BBB integrity. Copyright © 2014 Elsevier B.V. All rights reserved.
    Journal of Neuroimmunology 01/2015; 278C:30-43. DOI:10.1016/j.jneuroim.2014.11.023
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    ABSTRACT: Leukemia inhibitory factor (LIF) is known to potentiate the differentiation and survival of neuronal and oligodendrocyte precursors. Systemic therapy with LIF reportedly ameliorated the severity of experimental autoimmune encephalomyelitis and prevented oligodendrocyte death. We studied the secreted LIF levels from immune cells of relapsing remitting multiple sclerosis (RR-MS) patients compared to age- and gender-matched healthy controls (HCs). LIF was barely detected in the supernatants when the cells were not stimulated. After stimulation with anti-CD3/CD28 monoclonal antibody, LIF levels were up-regulated in both patients and controls, although to a significantly lower extent in RR-MS patients compared to HC. There were no significant differences between untreated patients and interferon-β1a treated patients. This is a heretofore unreported aspect of immune dysregulation in patients with RR-MS that may be related to insufficient remyelination and neurogenesis in MS lesions. Copyright © 2014 Elsevier B.V. All rights reserved.
    Journal of Neuroimmunology 01/2015; 278C:85-89. DOI:10.1016/j.jneuroim.2014.12.010
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    ABSTRACT: Myasthenia gravis (MG) is usually caused by antibodies against the muscle acetylcholine receptor (AChR). Plasmapheresis and immunoadsorption are often used to treat non-responsive patients. Antigen-specific immunoadsorption would remove only the pathogenic autoantibodies reducing side-effects. We expressed AChR extracellular domain mutants for use as specific adsorbents, and characterized them. Antigenicity and capacity for autoantibody binding were improved compared to the wild-type proteins. Adsorption appeared to be fast, as high plasma flow-rates could be applied. The bound autoantibodies were eluted repeatedly, allowing column reuse, without compromise in efficiency. Overall, the adsorbents were specific, efficient and suitable for use in therapy. Copyright © 2014 Elsevier B.V. All rights reserved.
    Journal of Neuroimmunology 01/2015; 278C:19-25. DOI:10.1016/j.jneuroim.2014.12.001
  • [Show abstract] [Hide abstract]
    ABSTRACT: The main aim of the study was to evaluate levels of cytokines IL-1ra, IL-2, IL-4, IL-6, IL-8, IL-10, IL-12, IL-17, TNF-alfa, TGB-beta1 and IFN-gamma in 30 patients with relapsing remitting (RRMS) compared to 30 secondary progressive multiple sclerosis (SPMS) in a peripheral blood sample. Statistical analysis showed significant higher levels of IL-17 and INF-gamma, which are cytokines with pro-inflammatory properties, and lower levels of TGF-beta1, a molecule with immunosuppressant activity, in RRMS compared to SPMS. These results underline the existence of a different cytokines dysregulation in RRMS compared to SPMS phases with higher pro-inflammatory activity in RRMS. Copyright © 2014. Published by Elsevier B.V.
    Journal of Neuroimmunology 01/2015; 278C:53-59. DOI:10.1016/j.jneuroim.2014.12.005