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A growing body of evidence suggests that angiogenesis plays a crucial role in the pathogenesis of multiple sclerosis (MS). Animal models of MS show a significant improvement when the process of angiogenesis is halted. In this study, we measured the serum levels of vascular-endothelial growth factor (VEGF), soluble Endoglin (sEng), angiopoietin 1(Ang-1), angiopoietin 2 (Ang-2), and uric acid (UA) as well as serum anti-Epstein-Barr virus (EBV) EBNA-1 IgG in 50 MS patients (including 20 newly diagnosed and 30 patients taking IFN-beta for >6months) and 40 healthy individuals. Enzyme-linked immunosorbent assays (ELISA) were used apart from UA where the uricase quantitative enzymatic assay was used. A significant increase of VEGF, Ang-1, Ang-2, and sEng in serum samples of MS patients with respect to healthy subjects was observed. VEGF was higher in newly diagnosed MS patients in comparison to patients taking interferon-beta and was associated with EDSS. The serum levels of UA were statistically lower in MS patients as compared to the healthy group. Higher levels of anti-EBV antibody titers were seen in MS patients than controls and anti-EBV titers correlated with angiogenic factors. It seems that in summary, angiogenesis may play an important role in MS and infection with EBV might be correlated with this phenomenon.

Multiple Sclerosis is a demyelinating disease of the central nervous system (CNS) affecting young individuals with age range of 20-40years of age. The precise mechanism underlying the disease is still unclear. Some viruses have been proposed to play roles in disease causation. In this study, we recruited 800 MS patients along with 1000 healthy individuals to determine the seropositivity of anti-CMV and anti-VZV IgG titers using enzyme-linked immunosorbent assay (ELISA). Our results showed significant higher titers of anti-CMV and anti-VZV IgG titers in serum of MS patients with respect to healthy individuals (for both p

Multiple sclerosis (MS) is a common inflammatory disease of the central nervous system unsurpassed for its variability in disease outcome. Apolipoprotein E (APOE) is involved in neuronal remodelling and several studies have attempted to examine the effect of APOE on MS disease severity, but its function in modifying the course of MS is controversial. It has been suggested recently that PVRL2, not APOE, is the locus on chromosome 19 which influences clinical outcome of MS. A cohort of sporadic MS cases, taken from opposite extremes of the putative distribution of long-term outcome using the most stringent clinical criteria to date, was used to determine the role of APOE and PVRL2 on MS disease severity. The MS cases selected represent the prognostic best 5% (benign MS) and worst 5% (malignant MS) of cases in terms of clinical outcome assessed by the EDSS. Genotyping the two sets of MS patients (112 benign and 51 malignant) and a replication cohort from Sardinia provided no evidence to suggest that APOE or PVRL2 have any outcome modifying activity. We conclude that APOE and PVRL2 have little or no effect on the clinical outcome of MS.

BACKGROUND: Incidence of multiple sclerosis is thought to be increasing, but this notion has been difficult to substantiate. In a longitudinal population-based dataset of patients with multiple sclerosis obtained over more than three decades, we did not show a difference in time to diagnosis by sex. We reasoned that if a sex-specific change in incidence was occurring, the female to male sex ratio would serve as a surrogate of incidence change. METHODS: Since environmental risk factors seem to act early in life, we calculated sex ratios by birth year in 27 074 Canadian patients with multiple sclerosis identified as part of a longitudinal population-based dataset. FINDINGS: The female to male sex ratio by year of birth has been increasing for at least 50 years and now exceeds 3.2:1 in Canada. Year of birth was a significant predictor for sex ratio (p

Vitamin D is being increasingly studied in multiple sclerosis (MS). A number of studies have shown that MS patients have lower levels of 25-hydroxyvitamin D as compared to comparator populations, but previous studies in Iran have been conflicting, perhaps due to their small sample size. We performed the largest study to date investigating 25-hydroxyvitamin D levels in Iranian MS patients (n=700) and controls (n=1000). 25-hydroxyvitamin D was measured using a quantitative chemiluminescent immunometric assay. 25-hydroxyvitamin D levels were lower in patients with MS. Over 24% of controls were vitamin D sufficient as compared to 3.4% of patients. Logistic regression showed that for every 1 ng/mL increase in 25-hydroxyvitamin D, the odds for MS decreased (odds ratio=0.87; 95% confidence interval (CI) 0.85-0.88; p0.001), after adjusting for age and sex. There was no association between 25-hydroxyvitamin D levels and disability scores in MS patients. Iranian Patients with MS have low levels of vitamin D and, where deemed necessary, appropriate supplementation should be given.

The precise aetiology of multiple sclerosis (MS) is yet to be conclusively determined, but both genes and environment and interactions thereof are important. It has been suggested that early life child exposure influences MS susceptibility. Here, in a population-based cohort, we investigated whether infant day care attendance influences the subsequent risk to develop MS. We identified 379 MS index cases and 101 spousal controls, all of whom were a single child (i.e. they had no biological sibs, half-sibs, step-sibs, adopted sibs) from the Canadian Collaborative Project on Genetic Susceptibility to MS (CCPGSMS). Frequency of infant day care attendance was compared for index cases and controls and the results were not statistically significant. Exposure to other infants during early childhood thus does not appear to be a risk factor for MS.

We read with interest the recent genome-wide association study by Li and colleagues and the identifi cation of single nucleotide polymorphisms (SNPs) in the glypican 5 (GPC5) gene associated with susceptibility to lung cancer in non-smokers. These variants were elegantly linked to the expression of GPC5, and this gene was also shown to be expressed at lower levels in lung cancer than in healthy lung tissue. The authors point out that diff erent SNPs in GPC5 have also been implicated in susceptibility to multiple sclerosis (MS). Intriguingly, a recent meta-analysis of cancer risk in MS has shown that the risk of all cancers (including lung cancer) is signifi cantly decreased in individuals with MS (odds ratio for all cancers 0·92, 95% CI 0·87–0·97). One study showed a particularly strongly decreased risk for cancers of the respiratory tract. This is at odds with a slightly increased risk for MS in smokers, although most patients with MS have not smoked. The SNPs implicated in lung cancer and MS are not in linkage disequilibrium with each other according to CEU HapMap data (r2