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Objectives: The aim of this study was to evaluate a short-term non-specific home-based 6-week cognitive training for its effect on neuropsychological deficits and depression., Subjects and Methods: Cognitive and affective abilities of patients with MS were compared with healthy controls using an identical neuropsychological test battery. Re-testing was performed after 6 weeks of cognitive home-based training., Results: Patients already showed cognitive deficits at baseline. Cognitive training resulted in a significant improvement in several skills, in particular with respect to visuoconstructive and figural long-term memory. In addition, prior depressed mood and quality of life improved in MS patients during the training period and remained up to 6 months., Conclusions: Our study corroborated the early appearance of neuropsychological deficits in MS. Mental training, although unspecific, lead to improvements with respect to attention and memory functions in patients, and to some degree in control subjects, which may last for more than 6 months., (Copyright 2008 S. Karger AG, Basel.)

Long-term development of psychological deficits in disability-free early multiple sclerosis (MS) was evaluated in 27 female patients over a period of 7 years and compared with healthy controls. Physical and cognitive parameters deteriorated significantly but not depression scores. In particular, the self-assessed somatic complaints remained non-similar between patients and controls. This indicates that although depression is clinically relevant and frequent in MS, in contrast to cognition it is not related to physical disease progression., (2004 S. Karger AG, Basel)

Neuromyelitis optica (NMO, or Devic's syndrome) is a rare syndrome characterized by the combination of acute or subacute optic neuritis and transverse myelitis. This strict confinement of lesions together with immunologic parameters such as frequent absence of oligoclonal banding despite increased signs of CSF inflammation suggest that NMO is distinct from multiple sclerosis (MS). Magnetic resonance imaging (MRI) data support NMO and MS as separate entities due to lesion distribution and signal characteristics. This is further supported by epidemiological and genetic evidence associating HLA-DRB1*1501 with disseminated "western" MS in contrast to NMO associated with DRB1*802, DPB1 501, and DPA1 202, the "Asian" type. Most findings suggest a heterogeneous pathogenesis of NMO and, in spite of the distinct localization, rather unspecific immune reactions seem to be involved. As to the frequent relapses of NMO, therapeutic options besides prednisolone are difficult to assess and favor long-term immune suppression or modulation.

We analyzed the sera of 51 patients with various phenotypes of X-linked adrenoleukodystrophy (X-ALD), 20 patients with multiple sclerosis (MS) and 22 healthy volunteers for the presence of autoantibodies specific for the recombinant extracellular immunoglobulin-like domain of human myelin oligodendrocyte glycoprotein (rhMOG(Igd)) and myelin basic protein (MBP). Anti-rhMOG(Igd) autoantibodies were significantly more frequent in X-ALD and MS patients as opposed to healthy individuals (p<0.05). Anti-MBP autoantibodies were present in about one-fourth of X-ALD and MS patients but in less than 10% of healthy individuals. Anti-rhMOG(Igd) autoantibody responses were not accompanied by increased T cell reactivity against rhMOG(Igd). These findings may have important implications for the understanding of humoral anti-myelin immunoreactivity in demyelinating diseases of the central nervous system such as X-ALD and MS.

Myelin-oligodendrocyte glycoprotein (MOG) specific antibodies (abs) are involved in autoantibody-mediated demyelination possibly contributing to lesion development in multiple sclerosis (MS). Interleukin-6 (IL-6) has been reported to play a crucial role for the pathogenesis of a MOG-induced animal model of MS. To investigate the link between anti-MOG abs production and IL-6 up-regulation in MS we determined the presence of anti-MOG abs and measured concentrations of IL-6 and its soluble receptors (sIL-6RC) in paired serum and cerebrospinal fluid (CSF) samples of MS patients and serum samples of age-matched healthy controls (HC). Anti-MOG abs were detected in 75% of MS sera, 57% of MS CSF samples and 20% of HC sera. There was no difference in IL-6 and sIL-6RC levels between anti-MOG abs positive and negative samples. Thus, no association between the presence of anti-MOG abs and serum/CSF levels of IL-6/sIL-6RC was found.

Antibodies directed against the extracellular immunoglobulin (Ig)-like domain of the myelin oligodendrocyte glycoprotein (MOG(Igd)) mediate demyelination in experimental autoimmune encephalomyelitis (EAE) and are implicated in the immunopathogenesis of multiple sclerosis (MS). In this study we investigated the epitope specificity of MOG(Igd)-specific autoantibodies immunopurified from MS patients (n=17) and normal healthy controls (HD; n=9). ELISA, using a panel of synthetic MOG(Igd) peptides, revealed that the epitope specificity of this response was heterogeneous in both groups. The most frequently recognised epitopes were located in amino acid sequences (a.a.) 1-26 (13/17) and 63-87 (15/17) in MS patients, and 14-39 (6/9) and 63-87 (6/9) in HDs, but there was no association between MS and any particular peptide specificity. We therefore investigated the ability of the immunopurified antibodies to recognise native MOG(Igd) expressed on at the membrane surface by FACS. Unexpectedly, antibodies fulfilling this essential criterion for a demyelinating antibody response were detected only in one of the MS samples. These results indicate that the epitope specificity of the human B cell response to MOG is not only heterogeneous, but may only mediate demyelination in a limited subset of MS patients.

We report a comparative study of the B- and T-cell responses to the extracellular immunoglobulin (Ig)-like domain of human myelin-oligodendrocyte glycoprotein (MOG(Igd)) in the blood of patients with multiple sclerosis and healthy controls using a bacterial recombinant human protein (rhMOG(Igd)). The frequency of anti-rhMOG(Igd)-seropositive samples, as determined by Western blotting, was significantly higher in the multiple sclerosis group (54%) than in normal random controls (excluding laboratory workers exposed to MOG) (22%; P = 0.02). In contrast, there was no difference in rhMOG(Igd)-induced proliferation indices of peripheral blood T cells between patients and controls. To characterize the rhMOG(Igd)-reactive T-cell repertoire, we isolated a panel of MOG-specific CD4(+) T-cell lines from multiple sclerosis patients and normal subjects, and these revealed a heterogeneous response with respect to epitope specificity, cytokine response, MHC (major histocompatibility complex) restriction and T-cell receptor Vbeta-chain usage. The majority of the T-cell lines recognized epitopes in the N-terminal region of MOG (amino acids 1-60). One epitope (represented by peptide 27-50) was exclusively recognized by T-cell lines from normal controls. Forty per cent of the MOG-specific T-cell lines analysed displayed a Th-2 or Th-0 cytokine profile and could therefore act as helper T cells in vivo.

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