H L Weiner

Brigham and Women's Hospital, Boston, Massachusetts, United States

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Publications (629)4091.06 Total impact

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    ABSTRACT: The objective of this study was to test a new version of the Magnetic Resonance Disease Severity Scale (MRDSS2), incorporating cerebral gray matter (GM) and spinal cord involvement from 3 T MRI, in modeling the relationship between MRI and physical disability or cognitive status in multiple sclerosis (MS). Fifty-five MS patients and 30 normal controls underwent high-resolution 3 T MRI. The patients had an Expanded Disability Status Scale score of 1.6±1.7 (mean±SD). The cerebral normalized GM fraction (GMF), the T2 lesion volume (T2LV), and the ratio of T1 hypointense LV to T2LV (T1/T2) were derived from brain images. Upper cervical spinal cord area (UCCA) was obtained from spinal cord images. A within-subject d-score (difference of MS from normal control) for each MRI component was calculated, equally weighted, and summed to form MRDSS2. With regard to the relationship between physical disability and MRDSS2 or its individual components, MRI-Expanded Disability Status Scale correlations were significant for MRDSS2 (r=0.33, P=0.013) and UCCA (r=-0.33, P=0.015), but not for GMF (P=0.198), T2LV (P=0.707), and T1/T2 (P=0.240). The inclusion of UCCA appeared to drive this MRI-disability relationship in MRDSS2. With regard to cognition, MRDSS2 showed a larger effect size (P=0.035) than its individual components [GMF (P=0.081), T2LV (P=0. 179), T1/T2 (P=0.043), and UCCA (P=0.818)] in comparing cognitively impaired with cognitively preserved patients (defined by the Minimal Assessment of Cognitive Function in MS). Both cerebral lesions (T1/T2) and atrophy (GMF) appeared to drive this relationship. We describe a new version of the MRDSS, which has been expanded to include cerebral GM and spinal cord involvement. MRDSS2 has concurrent validity with clinical status.
    Neuroreport 08/2014; · 1.40 Impact Factor
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    ABSTRACT: In the human disorder multiple sclerosis (MS) and in the model experimental autoimmune encephalomyelitis (EAE), macrophages predominate in demyelinated areas and their numbers correlate to tissue damage. Macrophages may be derived from infiltrating monocytes or resident microglia, yet are indistinguishable by light microscopy and surface phenotype. It is axiomatic that T cell-mediated macrophage activation is critical for inflammatory demyelination in EAE, yet the precise details by which tissue injury takes place remain poorly understood. In the present study, we addressed the cellular basis of autoimmune demyelination by discriminating microglial versus monocyte origins of effector macrophages. Using serial block-face scanning electron microscopy (SBF-SEM), we show that monocyte-derived macrophages associate with nodes of Ranvier and initiate demyelination, whereas microglia appear to clear debris. Gene expression profiles confirm that monocyte-derived macrophages are highly phagocytic and inflammatory, whereas those arising from microglia demonstrate an unexpected signature of globally suppressed cellular metabolism at disease onset. Distinguishing tissue-resident macrophages from infiltrating monocytes will point toward new strategies to treat disease and promote repair in diverse inflammatory pathologies in varied organs.
    The Journal of experimental medicine. 07/2014;
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    ABSTRACT: Patients with tuberous sclerosis complex (TSC) commonly present with significant neurologic deficits, including seizures, autism, and intellectual disability. Previous evidence suggests that the TSC2 mutation genotype may be associated with a more severe disease phenotype. This study evaluates the association of the TSC1 and TSC2 genotype with patient and disease characteristics in a retrospective review of a large TSC Natural History Database consisting of 919 patients with TSC.
    Epilepsia 06/2014; · 3.91 Impact Factor
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    ABSTRACT: The lack of prospective trial data comparing certain multiple sclerosis (MS) therapies could be addressed with observational research.
    Multiple sclerosis (Houndmills, Basingstoke, England). 05/2014;
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    ABSTRACT: To identify clinical and demographic features associated with the severity and recovery from acute optic neuritis (AON) episodes in patients with multiple sclerosis (MS).METHODS: Adult (n = 253) and pediatric (n = 38) patients whose first symptom was AON were identified from our MS database. Severity measured by loss of visual acuity (mild attack ≤20/40, moderate attack 20/50-20/190, and severe attack ≥20/200) and recovery in visual acuity at 1 year after the attack (complete recovery ≤20/20, fair recovery 20/40, and poor recovery ≥20/50) were recorded. Demographic and clinical features associated with attack severity and recovery were identified using proportional odds logistic regression. For another group of patients, blood samples were available within 6 months of an AON attack. In this group, the impact of vitamin D level on the severity/recovery was also assessed.RESULTS: Men (adjusted odds ratio [OR] = 2.28, p = 0.03) and subjects with severe attacks (adjusted OR = 5.24, p < 0.001) had worse recovery. AON severity was similar between the pediatric and adult subjects, but recovery was significantly better in pediatric subjects in the unadjusted analysis (p = 0.041) and the analysis adjusted for sex (p = 0.029). Season-adjusted vitamin D level was significantly associated with attack severity (OR for 10-U increase in vitamin D level = 0.47; 95% confidence interval: 0.32, 0.68; p < 0.001). Vitamin D level was not associated with recovery from the attack (p = 0.98) in univariate analysis or after accounting for attack severity (p = 0.10).CONCLUSION: Vitamin D levels affect AON severity, whereas younger age, attack severity, and male sex affect AON recovery. Underlying mechanisms and potential therapeutic targets may identify new measures to mitigate disability accrual in MS.
    Neurology 05/2014; · 8.25 Impact Factor
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    ABSTRACT: Gonadal steroids may modulate disease course in multiple sclerosis (MS). To assess the prevalence and clinical associations of hypogonadism in men with MS. Male patients, aged 18-65 years, with relapsing-remitting MS (RRMS) or clinically-isolated syndrome (CIS) and their first symptom < 10 years prior were selected from a longitudinal clinical study. We measured their hormones in stored morning blood samples, and collected their Expanded Disability Status Scale (EDSS) scores every 6 months and their Symbol Digit Modalities Test (SDMT) results annually. Our analysis included 96 men with a mean age of 40 years, EDSS of 1.1 and disease duration of 4.6 years. Of these men, 39% were hypogonadal (total testosterone < 288 ng/dL); none showed compensatory elevations in luteinizing hormone. Their low testosterone levels and testosterone:estradiol ratios were negatively correlated with body mass index (BMI) and leptin, and showed no correlation with 25-hydroxy-vitamin D levels. In our primary cross-sectional analyses, there was a negative age-adjusted correlation between total testosterone and EDSS (p = 0.044). In the age-adjusted longitudinal analyses, higher baseline testosterone levels were associated with less decline in SDMT (p = 0.012). Men with MS may experience hypogonadotropic hypogonadism. Low testosterone levels may be associated with worse clinical outcomes. A potential neuroprotective role for testosterone warrants further investigation.
    Multiple Sclerosis 04/2014; · 4.47 Impact Factor
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    ABSTRACT: Objectives Patients with tuberous sclerosis complex (TSC) frequently have autism spectrum disorders and neuropsychiatric disorders. Subependymal giant cell astrocytomas (SEGAs) have been reported to occur in 5–20% of patients with TSC; however, the relationship between SEGAs and neuropsychiatric disorders in TSC remains unknown. We utilized a large multicenter database to study associations between SEGAs and neuropsychiatric disorders in patients with TSC.Methods Associations between the presence of SEGAs and neuropsychiatric disorders were examined in a retrospective review of 916 patients enrolled in the TSC Natural History Database Project (Tuberous Sclerosis Alliance).ResultsAmong the 916 TSC patients, 226 had SEGAs (25%) and 155 had autism spectrum disorder (ASD) (17%). Compared to patients without SEGAs, patients with SEGAs were 1.83 (95% confidence interval [CI] 1.26–2.66) times more likely to have ASD. No significant relationship was found between SEGAs and intellectual disability, attention-deficit/hyperactive disorder, or major depressive disorder.SignificanceThe clinical presentation of TSC is highly variable and not well understood. These data show that SEGAs are associated with ASD in patients with TSC, suggesting that the pathologic changes leading to SEGA formation may also predispose patients to ASD.A PowerPoint slide summarizing this article is available for download in the Supporting Information section here.
    Epilepsia 04/2014; · 3.96 Impact Factor
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    ABSTRACT: More than 80% of the human genome is biochemically active, whereas less than 3% of the genome encodes proteins. The emerging field of non-coding ribonucleic acids (RNAs) that are products of the genome, but do not program proteins, has revolutionized our understanding of cell biology. This was followed by a growing interest in the role of non-coding RNAs in the pathogenesis of human diseases, including multiple sclerosis (MS). In April 2013, a symposium in Warsaw, Poland, was the first meeting entirely dedicated to advances in the understanding of the roles of various subclasses of non-coding RNAs and showcased their involvement in autoimmune demyelination and MS. New mechanisms of action of small non-coding RNAs, as well as the advent of long non-coding RNAs were discussed, including the potential role of non-coding RNAs as MS biomarkers and their use for therapeutic intervention in MS.
    Multiple Sclerosis 02/2014; · 4.47 Impact Factor
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    ABSTRACT: Genetic loss of Tsc1/Tsc2 function in tuberous sclerosis complex (TSC) results in altered mammalian target of rapamycin (mTOR) signaling and abnormal brain development. Although earlier studies have focused on characterization of cortical tubers, in this study we sought to examine the unique cellular and molecular features of the perituberal cortex in order to better understand its contribution to epileptogenesis, cognitive dysfunction, and autism. Standard histologic and immunohistochemical labeling was used to assess structural abnormalities and cell-specific pattern of mTORC1 activation in surgically resected cortical tubers and perituberal cortex. Western blotting was performed to quantify the expression of the mTORC1 and mTORC2 biomarkers phospho-S6 (Ser235/236), phospho-S6 (Ser240/244), and phospho-Akt (Ser473), in addition to evaluating the differential expression levels of several neuronal and glial-specific proteins in tubers and peritubers, as compared to non-TSC epilepsy specimens. Tubers demonstrated mild to severe disruption of cortical lamination, the presence of pS6-positive dysplastic neurons and giant cells, an overall increase in mTORC1 and a decrease in mTORC2 activity, increased axonal connectivity and growth, and hypomyelination. Perituberal cortex presented similar histologic, immunohistochemical, and molecular features; however, they were overall milder. Axonal growth was specific for TSC and was negatively correlated with deficient myelination. Our results show an extension of cellular dysplasia and dysregulated mTOR signaling in the perituberal tissue, and demonstrate for the first time aberrant connectivity in human TSC brain. This study provides new insights into the pathophysiology of neurologic dysfunction associated with TSC and supports the intrinsic epileptogenicity of normal-appearing perituberal cortex.
    Epilepsia 02/2014; · 3.96 Impact Factor
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    ABSTRACT: Sturge-Weber syndrome (SWS) is a neurocutaneous disorder comprised typically of a facial nevus, leptomeningeal angioma with calcifications, and seizures. SWS without a port-wine stain is a rare variant with only 30 cases reported in the literature. Here, a case of an 8-year-old girl with no cutaneous abnormalities presenting with medically intractable epilepsy and MRI and CT findings consistent with SWS is described. The patient underwent multistage surgery with subdural electrode monitoring before and after resection of the epileptogenic focus, with complete excision of the lesion and postoperative resolution of her seizures. This is the first reported case of three-stage surgery for localized resection of the seizure focus for SWS. © 2014 S. Karger AG, Basel.
    Pediatric Neurosurgery 01/2014; · 0.42 Impact Factor
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    ABSTRACT: Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS) considered to be a T cell-mediated autoimmune disease. Mucosally administered antigens induce regulatory T cells that secrete anti-inflammatory cytokines at the anatomic site where the mucosally administered Ag is located. We have previously reported in a mouse model of stroke that nasal treatment with MOG35-55 peptide reduces ischemic infarct size and improves behavior, by inducing IL-10-secreting T cells. We have also demonstrated that an experimental autoimmune encephalomyelitis (EAE) model in non-obese diabetic (NOD) mice leads to a relapsing progressive disease and that brain lesions can be visualized noninvasively by magnetic resonance imaging (MRI). Here, we investigated whether nasal treatment with 25 μg of MOG35-55 after the first attack affects clinical progression and MRI outcome in the NOD model. We found that nasal MOG35-55 treatment administered three times after the first attack and then weekly reduced both the peak clinical disease score and clinical score during remission. Pathology revealed less infiltration of cells and reduction in white-matter damage as measured by Luxol blue staining in treated animals. This model is unique in that there are lesions in the corpus callosum, external capsule, fimbria, internal capsule and thalamus, which is analogous to what is observed in MS. MRI of individual animals using fractional anisotropy (FA) and T1-gadolinum (T1-Gd) imaging was able to identify lesions in all of these anatomic areas, and we found lower levels of brain pathology by MRI in treated mice with both methods. Our results indicate a beneficial effect of nasal MOG on relapsing-progressive EAE and demonstrate that non-invasive MRI imaging may be used to monitor treatment of ongoing disease in this model for testing new therapies for MS.
    Experimental Neurology 01/2014; · 4.65 Impact Factor
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    ABSTRACT: Disease-modifying therapies (DMTs) for the treatment of multiple sclerosis (MS) are associated with inconvenient methods of administration, significant side effects, and low adherence rates. This study was undertaken to compare treatment satisfaction in MS patients treated with interferon beta-1a intramuscular (IFNβ-1a IM), interferon beta-1a subcutaneous (IFNβ-1a SC), glatiramer acetate (GA), and natalizumab (NTZ), and to examine the associations between treatment satisfaction ratings and adherence to therapy.
    International journal of MS care. 01/2014; 16(2):68-75.
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    ABSTRACT: Dendritic cells (DCs) serve a critical role both in promoting and inhibiting adaptive immunity. The goal of this study was to investigate the effect of natalizumab (NTZ) treatment on DC numbers, phenotype, and function in patients with multiple sclerosis (MS).
    PLoS ONE 01/2014; 9(7):e103716. · 3.73 Impact Factor
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    ABSTRACT: Microglia are myeloid cells of the CNS that participate both in normal CNS function and in disease. We investigated the molecular signature of microglia and identified 239 genes and 8 microRNAs that were uniquely or highly expressed in microglia versus myeloid and other immune cells. Of the 239 genes, 106 were enriched in microglia as compared with astrocytes, oligodendrocytes and neurons. This microglia signature was not observed in microglial lines or in monocytes recruited to the CNS, and was also observed in human microglia. We found that TGF-β was required for the in vitro development of microglia that express the microglial molecular signature characteristic of adult microglia and that microglia were absent in the CNS of TGF-β1-deficient mice. Our results identify a unique microglial signature that is dependent on TGF-β signaling and provide insights into microglial biology and the possibility of targeting microglia for the treatment of CNS disease.
    Nature Neuroscience 12/2013; · 15.25 Impact Factor
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    ABSTRACT: Leptin and A-FABP are produced by white adipose tissue and may play a role in chronic inflammation in MS. To assess the leptin and adipocyte-fatty acid binding protein (A-FABP)in relapsing and progressive forms of MS. Adipokine levels were measured in untreated adult relapsing-remitting MS (RRMS), secondary progressive MS (SPMS), primary progressive MS (PPMS) and healthy controls. Pediatric-onset MS (POMS) and pediatric healthy controls (PHC) were also assessed. Leptin and A-FABP levels were measured in serum by ELISA. Groups were compared using linear mixed-effects model. Excluding two patients with BMI > 50, a significant difference in leptin level was found between RRMS and HC controlling for age (p = 0.007), SPMS and HC controlling for age alone (p = 0.002), or age and BMI (p = 0.007). A-FABP levels were higher in SPMS than HCs (p = 0.007), controlling for age and BMI. Differences in A-FABP levels between POMS and PHC was observed after controlling for age (p = 0.019), but not when BMI was added to the model (p = 0.081). Leptin and A-FABP levels are highest in SPMS compared to HC, suggesting a role in pathogenesis of this disease subtype. A-FABP levels are increased in POMS patients and may play a role in the early stages of disease.
    BMC Neurology 11/2013; 13(1):172. · 2.56 Impact Factor
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    ABSTRACT: Object Subependymal giant cell astrocytomas (SEGAs) are benign tumors, most commonly associated with tuberous sclerosis complex (TSC). The vast majority of these tumors arise from the lateral ependymal surface adjacent to the foramen of Monro, therefore potentially encroaching on one or both foramina, and resulting in obstructive hydrocephalus that necessitates surgical decompression. The indications for surgery, intraoperative considerations, and evolution of the authors' management paradigm are presented. Methods Patients with TSC who underwent craniotomy for SEGA resection at New York University Langone Medical Center between January 1997 and March 2011 were identified. Preoperative imaging, clinical characteristics, management decisions, operative procedures, and outcomes were reviewed. Results Eighteen patients with TSC underwent 22 primary tumor resections for SEGAs. The indication for surgery was meaningful radiographic tumor progression in 16 of 21 cases. The average age at the time of operation was 10.3 years. Average follow-up duration was 52 months (range 12-124 months). The operative approach was intrahemispheric-transcallosal in 16 cases, transcortical-transventricular in 5, and neuroendoscopic in 1. Nine tumors were on the right, 9 on the left, and 3 were bilateral. Gross-total resection was documented in 16 of 22 cases in our series, with radical subtotal resection achieved in 4 cases, and subtotal resection (STR) in 2 cases. Two patients had undergone ventriculoperitoneal shunt placement preoperatively and 7 patients required shunt placement after surgery for moderate to severe ventriculomegaly. Two patients experienced tumor progression requiring reoperation; both of these patients had initially undergone STR. Conclusions The authors present their management strategy for TSC patients with SEGAs. Select patients underwent microsurgical resection of SEGAs with acceptable morbidity. Gross-total resection or radical STR was achieved in 90.9% of our series (20 of 22 primary tumor resections), with no recurrences in this group. Approximately half of our patient series required CSF diversionary procedures. There were no instances of permanent neurological morbidity associated with surgery.
    Journal of Neurosurgery Pediatrics 11/2013; · 1.63 Impact Factor
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    ABSTRACT: We set out to characterize the clinical impact and functional consequences of rs1800693(G), the multiple sclerosis (MS) susceptibility allele found in the TNFRSF1A locus. We analyzed prospectively collected data on patients with MS to assess the role of the TNFRSF1A locus on disease course and treatment response. Using archival serum samples and freshly isolated monocytes from patients with MS and healthy subjects, we evaluated the effects of rs1800693(G) and a second risk allele, R92Q, on immune function. In 772 patients with MS, we see no evidence that rs1800693(G) strongly influences clinical or radiographic indices of disease course and treatment response; thus, rs1800693(G) appears to be primarily involved in the onset of MS. At the molecular level, this validated susceptibility allele generates an RNA isoform, TNFRSF1A Δ6, that lacks the transmembrane and cytoplasmic domains. While there was no measurable effect on serum levels of soluble TNFRSF1A, rs1800693(G) appears to alter the state of monocytes, which demonstrate a more robust transcriptional response of CXCL10 and other genes in response to tumor necrosis factor (TNF)-α. We also report that activation of the TNF-α pathway results in altered expression of 6 other MS susceptibility genes, including T-cell activation rho GTPase activating protein (TAGAP) and regulator of G-protein signaling 1 (RGS1), which are not previously known to be responsive to TNF-α. The MS rs1800693(G) susceptibility allele affects the magnitude of monocyte responses to TNF-α stimulation, and the TNF pathway may be one network in which the effect of multiple MS genes becomes integrated.
    Neurology 10/2013; · 8.25 Impact Factor
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    ABSTRACT: Surgical resection of epileptic foci relies on accurate localization of the epileptogenic zone, often achieved by subdural and depth electrodes. Our epilepsy center has treated selected children with poorly localized medically refractory epilepsy with a staged surgical protocol, with at least one phase of invasive monitoring for localization and resection of epileptic foci. To evaluate the safety of staged surgical treatments for refractory epilepsy among children. Data were retrospectively collected, including surgical details and complications of all patients who underwent invasive monitoring. 161 children underwent 200 admissions including staged procedures (>1 surgery during one hospital admission), and 496 total surgeries. Average age at surgery was 7y (8m-16.5y). 250 surgeries included resections (and invasive monitoring), and 189 involved electrode placement only. Cumulative total number of surgeries per patient was 2-10 (average 3). Average duration of monitoring was 10 days (1-30). There were no deaths. Follow-up ranged from 1m to 10y. Major complications included unexpected new permanent mild neurological deficits (2%/admission), CNS or bone flap infections (1.5%/admission), intracranial hemorrhage, CSF leak, and a retained strip (each 0.5%/admission). Minor complications included bone absorption (5%/admission), positive surveillance sub/epidural cultures in asymptomatic patients (5.5%/admission), non-infectious fever (5%/admission), and wound complications (3%/admission). 30 complications necessitated additional surgical treatment. Staged epilepsy surgery, with invasive electrode monitoring, is safe in children with poorly localized medically refractory epilepsy. The rate of major complications is low, and appears comparable to that associated with other elective neurosurgical procedures.
    Neurosurgery 10/2013; · 2.53 Impact Factor
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    ABSTRACT: Tuberous sclerosis complex is an autosomal dominant disorder predisposing to the development of benign lesions in different body organs, mainly in the brain, kidney, liver, skin, heart, and lung. Subependymal giant cell astrocytomas are characteristic brain tumors that occur in 10% to 20% of tuberous sclerosis complex patients and are almost exclusively related to tuberous sclerosis complex. Subependymal giant cell astrocytomas usually grow slowly, but their progression ultimately leads to the occlusion of the foramen of Monro, with subsequent increased intracranial pressure and hydrocephalus, thus necessitating intervention. During recent years, secondary to improved understanding in the biological and genetic basis of tuberous sclerosis complex, mammalian target of rapamycin inhibitors have been shown to be effective in the treatment of subependymal giant cell astrocytomas, becoming an alternative therapeutic option to surgery. In June 2012, an International Tuberous Sclerosis Complex Consensus Conference was convened, during which an expert panel revised the diagnostic criteria and considered treatment options for subependymal giant cell astrocytomas. This article summarizes the subpanel's recommendations regarding subependymal giant cell astrocytomas. Mammalian target of rapamycin inhibitors have been shown to be an effective treatment of various aspects of tuberous sclerosis complex, including subependymal giant cell astrocytomas. Both mammalian target of rapamycin inhibitors and surgery have a role in the treatment of subependymal giant cell astrocytomas. Various subependymal giant cell astrocytoma-related conditions favor a certain treatment.
    Pediatric Neurology 10/2013; · 1.42 Impact Factor
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    ABSTRACT: Osteopontin (OPN) is a pleiotropic protein with important roles in inflammation and immunity that has been suggested as a candidate biomarker for disease activity in multiple sclerosis (MS). We evaluated plasma levels of OPN in an unselected cohort of MS patients, to determine its potential as a biomarker for disease subtype and/or disease activity in a regular clinical setting. We analyzed OPN plasma levels in 492 consecutive MS patients, using a commercial enzyme-linked immunosorbent assay (ELISA). OPN levels were higher in relapsing-remitting and secondary progressive MS, compared to healthy controls. Treatment with natalizumab or glatiramer acetate was associated with lower OPN levels. There was no significant association between the OPN levels and disease activity, as measured by clinical or radiological criteria. One-third of patients with high OPN levels had concurrent disorders that may also be associated with increased OPN expression, and which may mask a modest effect of MS disease activity on OPN levels. Our data do not support a role for circulating OPN levels as a biomarker for disease activity in a heterogeneous clinical setting, but does not rule out a potential role in the cerebrospinal fluid, in a controlled setting such as a clinical trial, or in concert with other biomarkers.
    Multiple Sclerosis 09/2013; · 4.47 Impact Factor

Publication Stats

35k Citations
4,091.06 Total Impact Points

Institutions

  • 1983–2014
    • Brigham and Women's Hospital
      • • Center for Neurologic Diseases
      • • Department of Medicine
      • • Center of Multiple Sclerosis
      • • Center for Brain Mind Medicine
      Boston, Massachusetts, United States
    • Dana-Farber Cancer Institute
      Boston, Massachusetts, United States
  • 1978–2014
    • Harvard Medical School
      • • Department of Neurology
      • • Department of Medicine
      • • Department of Genetics
      Boston, Massachusetts, United States
  • 2013
    • Children's Hospital Los Angeles
      Los Angeles, California, United States
  • 1988–2013
    • Massachusetts General Hospital
      • • Department of Neurology
      • • Department of Pathology
      Boston, MA, United States
  • 1983–2012
    • Boston Children's Hospital
      • • Department of Neurology
      • • Department of Radiology
      • • Children's Hospital Primary Care Center
      Boston, MA, United States
  • 2011
    • University of Massachusetts Boston
      Boston, Massachusetts, United States
    • Tel Aviv University
      • Department of Neurology
      Tel Aviv, Tel Aviv, Israel
  • 1999–2011
    • NYU Langone Medical Center
      • • Division of Pediatric Surgery
      • • Department of Neurology
      New York City, NY, United States
    • Hospital Italiano de Buenos Aires
      Buenos Aires, Buenos Aires F.D., Argentina
  • 2010
    • Rutgers New Jersey Medical School
      • Division of Neurology
      Newark, NJ, United States
    • Memorial Sloan-Kettering Cancer Center
      New York City, New York, United States
  • 2009
    • Weill Cornell Medical College
      New York City, New York, United States
  • 1999–2007
    • New York University
      • School of Medicine NYU Langone Medical Center
      New York City, New York, United States
  • 2006
    • Ben-Gurion University of the Negev
      • Faculty of Health Sciences
      Beersheba, Southern District, Israel
    • Federal University of Minas Gerais
      • Departamento de Bioquímica e Imunologia
      Belo Horizonte, Estado de Minas Gerais, Brazil
  • 1993–2006
    • State University of New York Downstate Medical Center
      • • Department of Neurosurgery
      • • Division of Pediatric Surgery
      Brooklyn, NY, United States
    • Beth Israel Deaconess Medical Center
      • Department of Medicine
      Boston, MA, United States
  • 2003
    • Universitätsklinikum Münster
      Muenster, North Rhine-Westphalia, Germany
  • 2001–2003
    • CUNY Graduate Center
      New York City, New York, United States
  • 2002
    • Stanford University
      • Department of Neurosurgery
      Stanford, CA, United States
    • New York Presbyterian Hospital
      New York City, New York, United States
    • University of Münster
      Muenster, North Rhine-Westphalia, Germany
  • 2000
    • Comprehensive Cancer Centers of Nevada
      Las Vegas, Nevada, United States
    • Harvard University
      Cambridge, Massachusetts, United States
  • 1994
    • Carmel Medical Center
      H̱efa, Haifa District, Israel
    • Hebrew University of Jerusalem
      • Department of Animal Sciences
      Yerushalayim, Jerusalem District, Israel
  • 1992–1993
    • Alfred Hospital
      Melbourne, Victoria, Australia
  • 1990
    • National Institutes of Health
      • Laboratory of Immunology
      Bethesda, MD, United States