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Investigators have reported finding traces of Epstein-Barr virus in postmortem brains examined from people with different forms of MS. They found the traces of EBV infection in immune cells (B cells and plasma cells) that had infiltrated the brain in 21 out of 22 brains from people with MS, but not in brains from people who had other neurological diseases that, like MS, involve inflammation.
If these exciting findings are confirmed by other laboratories, they add to growing evidence of a link between EBV and MS. However, it is not possible through this study to determine whether EBV causes MS, or whether its presence is a consequence of MS. This merely adds to evidence of a linkage between EBV and MS, but does not prove EBV causes MS.
Epstein-Barr virus is a herpes virus known to cause infectious mononucleosis (often called glandular fever) and other disorders. Most people in the general population have been exposed to the virus. After an initial infection EBV becomes latent or dormant, and can be reactivated. EBV infects B cells, the cells of the immune system that make antibodies. There is currently no vaccine that can protect against an initial infection by EBV, and no anti-viral medication that can fight the active infection or kill latent virus harbored in the body. This virus does not infect other species, so research on EBV can only be carried out in humans.
The cause of MS, an unpredictable immune-mediated disease that attacks the central nervous system, is unknown, but the disease is thought to occur when susceptible individuals encounter a triggering factor or factors in their environment. Several previous studies have suggested a possible link between EBV and MS, but other infectious agents have also been linked to MS, leading some researchers to suggest that the way the immune system responds to infections, rather than the infectious agent itself, may lead to the onset of MS. Previous examinations of MS brain tissue for signs of EBV have been for the most part negative. In a report published last year, the US National MS Society-supported investigators showed evidence that individuals who had signs of significant exposure to EBV were twice as likely to develop multiple sclerosis up to 20 years later.
Reference: Serafini, B et al. (2007) Dysregulated Epstein-Barr virus infection in the multiple sclerosis brain. Journal of Experimental Medicine 5 Nov 2007.
Read abstract/source full text of article: http://highwire.stanford.edu/cgi/medline/pmid;17984305
Researchers say that cognitive deficits in MS are common and correlate with contemporary MRI brain abnormalities, particularly atrophy, but the ability of imaging early in the disease to predict later cognitive impairment remains to be determined.
This team assessed 30 people with relapsing-remitting MS recruited within three years of disease onset, and in whom MRI had been performed at baseline and a year later.
The results suggest that neuroaxonal loss was identified early in the disease, and its rate of progression, predicted cognitive impairment later in the disease. They suggest neuroaxonal loss is likely to affect the nerve fibres that subserve the cognitive processes impaired in MS.
Reference: Ron, M (2007) Cognitive impairment in relapsing-remitting multiple sclerosis can be predicted by imaging performed several years earlier. Multiple Sclerosis 6 Nov 2007.
Read abstract/source full text of article: http://highwire.stanford.edu/cgi/medline/pmid;17986503
This team of researchers notes that although the pathogenesis of MS is not yet completely understood, various studies suggest that immune-mediated loss of myelin and mitochondrial dysfunction are associated with the disease.
Mitochondria are one of the main cellular sources of reactive oxygen species (ROS) and reactive nitrogen species (RNS) and play a pivotal role in many neuro-pathological conditions.
Mitochondrial dysfunction leading to excessive production of ROS and RNS plays a significant role in the pathogenesis of MS, particularly in loss of myelin/oligodendrocyte complex.
This review summarizes critical role of mitochondria in the pathogenesis of MS. Further understanding of the role of mitochondria in MS, they say, may provide rationale for novel approaches to this disease and development of novel therapeutic maneuvers.
Reference: Ghafourifar, P. et al. (2007) Mitochondria in multiple sclerosis. Frontiers in Biosciencei 1 Jan 2008 13: p. 3116.
Read abstract/source full text of review: http://highwire.stanford.edu/cgi/medline/pmid;17981781
Canadian researchers note that randomised controlled trials incorporating validated depression scales have failed to identify an association between interferon beta treatment and depression in MS.
They say that this is surprising since interferons used in other clinical contexts are considered capable of causing depression.
They analysed a database containing information about antidepressant prescriptions filled at outpatient pharmacies in Canada which they used as a proxy indicator for depressive disorders.
The frequency of antidepressant use was compared in cohorts treated with glatiramer acetate and interferon beta.
They concluded there was no evidence that antidepressant treatment occurs more often in people treated with interferon beta than in those treated with glatiramer acetate. These results help to confirm that depression is not associated with interferon beta treatment in MS.
Reference: Patten, S., Williams, J. and Metz, L. (2007) Anti-depressant use in association with interferon and glatiramer acetate treatment in multiple sclerosis. Multiple Sclerosis 6 Nov 2007.
Read abstract/source full text of article: http://highwire.stanford.edu/cgi/medline/pmid;17986504
Researchers have observed that HLA-DRB1* 15 increases risk of MS in people of Northern European descent.
In this investigation of 7,334 individuals from 1,515 MS families, the largest cohort used to study the HLA-DRB1 locus to date, investigators analysed the transmission of HLA-DRB1*15 stratified by sex of transmitting parent.
A significant over transmission of HLA-DRB1*15 from mothers was observed, suggesting that parent of origin may determine susceptibility to MS.
Reference: Sreeram V Ramagopalan, S. et al. (2007) Parental transmission of HLA-DRB1*15 in multiple sclerosis. Human Genetics 31 Oct 2007.
Read abstract/source full text of article: http://highwire.stanford.edu/cgi/medline/pmid;17972102