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Background The first years of relapsing-remitting multiple sclerosis (RRMS) constitute the most vulnerable phase for the progression of cognitive impairment (CImp), due to a gradual decrease of compensatory mechanisms. In the first 10 years of RRMS, the temporal volumetric changes of deep gray matter structures must be clarified, since they could constitute reliable cognitive biomarkers for diagnostic, prognostic, and therapeutic purposes. Methods Forty-five cognitively asymptomatic patients with RRMS lasting ≤ 10 years, and with a brain MRI performed in a year from the neuropsychological evaluation (Te-MRI), were included. They performed the Brief International Cognitive Assessment battery for MS. Thirty-one brain MRIs performed in the year of diagnosis (Td-MRI) and 13 brain MRIs of age- and sex-matched healthy controls (HCs) were also included in the study. The relationships between clinical features, cognitive performances, and Te- and Td-MRI volumes were statistically analyzed. Results Cognitively preserved (CP) patients had significantly increased Td-L-putamen (P = 0.035) and Td-R-putamen volume (P = 0.027) with respect to cognitively impaired (CI) ones. CI patients had significantly reduced Te-L-hippocampus (P = 0.019) and Te-R-hippocampus volume (P = 0.042) compared, respectively, with Td-L-hippocampus and Td-R-hippocampus volume. Td-L-putamen volume (P = 0.011) and Te-L-hippocampus volume (P = 0.023) were independent predictors of the Symbol Digit Modalities Test score in all patients (r2 = 0.31, F = 6.175, P = 0.001). Conclusion In the first years of RRMS, putamen hypertrophy and hippocampus atrophy could represent promising indices of cognitive performance and reserve, and become potentially useful tools for diagnostic, prognostic, and therapeutic purposes.

Background: Cerebrospinal fluid (CSF) analysis in patients with particular neurologic disorders is a powerful tool to evaluate specific central nervous system inflammatory markers for diagnostic needs, because CSF represents the specific immune micro-environment to the central nervous system. Methods: CSF samples from 49 patients with multiple sclerosis (MS), Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) and non-inflammatory neurologic disorders (NIND) as controls were submitted to protein expression profiles of 47 inflammatory biomarkers by multiplex Luminex bead assay to investigate possible differences in the inflammatory process for MS and CIDP. Results: Our results showed differences in CSF cytokine levels in MS and CIDP, in particular IL12 (p40) was significantly highly expressed in MS in comparison with CIDP and NIND, while SDF-1 and SCGF- were significantly highly expressed in CIDP cohort when compared to MS and NIND. IL-9, IL-13, and IL-17 had higher expression levels in NIND if compared with the other groups. Conclusions: Our study showed that, despite some common pathogenic mechanisms, central and peripheral nervous system demyelinating diseases, such as MS and CIDP, differ in some specific inflammatory soluble proteins in CSF, underlining differences in the immune response involved in those autoimmune diseases

A polymorphism (PM) in the microsatellite of the promoter region of matrix metalloproteinase 9 (MMP-9), modulating its expression, could play a role in susceptibility to multiple sclerosis (MS). MMP-9 PM was determined in 95 patients with MS (MS Group) and 95 ageand sex-matched controls (Control Group). Comparison of allelic frequencies showed that a higher number of CA repeats characterized the MS group ( P < 0.0001) and prevalence of carriers of z22 CA repeats was higher in the MS than in the Control Group (OR 3.4, 95% CI: 1.7–6.8, P < 0.0001). An earlier age at disease onset was a characteristic of patients with >22 CA repeats (33F10 vs. 28F10, P= 0.027). No differences were found in the main MRI parameters.

The objective of the study was to examine the relationship between HLA genotypes and disease severity as measured by brain MRI quantitative markers of demyelinating and destructive pathology in patients with multiple sclerosis (MS). We studied 100 patients with MS and 122 age, sex-, ethnic- and residence-matched controls. The DNA extraction and the genomic typing (A, B, DRB1 and DQB1 loci) were obtained with sequence-specific oligonucleotide method, using a commercially available reversible line blot assay (INNO-LIPA). All patients underwent a 1.5 tesla MRI examination of the brain. Disease severity was assessed by clinical (Expanded Disability Status Scale (EDSS)) and MRI (T2- and T1-lesion load (LL) and brain parenchymal fraction (BPF)) outcome measures. HLA-DQB1* 02 (OR 19.9, 95% C. I. 16.2-24.3, uncorrected (uncorr)- p

To establish the relationship between the presence and titer of virus-specific serum- and cerebrospinal fluid (CSF)-antibodies in multiple sclerosis (MS) patients and disease severity measured with different quantitative magnetic resonance imaging (MRI) techniques.We investigated an association between clinical and MRI measures of disease activity and the presence and titer of IgG antibodies against seven common viruses (measles, rubella, herpes simplex virus type 1 and 2, varicella zoster virus, cytomegalovirus (CMV) and Epstein-Barr virus). One hundred and forty (90 female/50 male) patients with definite MS and 131 age and sex-matched controls participated in the study. Antibody positivity and titer were ascertained by the enzyme linked immunosorbent assay (ELISA) technique and clinical assessment was performed by evaluating the expanded disability status scale (EDSS) score and the lifetime relapse rate (LRR). T1- and T2-lesion loads (LL) and the brain parenchymal fraction (BPF) were calculated.Multiple analyses showed that there was an association between antibody positivity against CMV and higher titer and better clinical and MRI outcomes. The cluster analyses indicated that patients positive for antibodies against CMV had significantly older age at onset (uncorr p = 0.001 and corr p = 0.009), lower LRR (uncorr p = 0.003 and corr p = 0.03) and higher BPF (uncorr p = 0.004 and pcorr p = 0.04). CMV-positive patients who had higher antibody titer showed lower T2-LL (uncorr p = 0.003 and corr p = 0.03) and higher BPF (uncorr p = 0.006 and corr p = 0.05).Surprisingly, our results focused attention on the 'protective' role of a particular virus. CMV is probably capable of triggering some immunomodulating/immune evasion mechanisms which may decrease immune reactivity in MS patients. Further studies are needed to confirm and elucidate our study results on a larger sample of MS patients and in animal model studies.