Methionine metabolism and multiple sclerosis.

Context: Methylation reactions are particularly important in the brain and their inhibition can lead to a number of serious pathologies. Multiple sclerosis is one of the most common neurological disorders caused by interaction of genetic and environmental factors, but little is known about its cause or factors that contribute to the disorder. Although multiple sclerosis is primarily regarded as demyelinating disorder, there are no many articles focusing on methionine determination.

Changes in levels of oxidative stress markers and some neuronal enzyme activities in cerebrospinal fluid of multiple sclerosis patients.

Objectives: The aim of the present study was to assess cerebrospinal fluid (CSF) levels of malondialdehyde (MDA), F2 isoprostanes (8-iso-PGF2α) and total antioxidant status (TAS) in relapsing-remitting (RR) and secondary progressive (SP) course of MS and neurological controls. These parameters were correlated with brain tissue damage parameters - neuron-specific enolase and 3´,5´-cAMP-phosphodiesterase (PDE) in CSF.

Methods: CSF samples were obtained from MS patients divided into two groups according to the disease severity (EDSS) - RR and SP course of MS.

Role of astrocytes in pathogenesis of multiple sclerosis and their participation in regulation of cerebral circulation.

There is about 30% higher risk of the myocardial infarction in patients diagnosed with multiple sclerosis (MS) than in people without MS. Increased risk of cardiovascular disease development positively correlates with levels of serum markers of an endothelial dysfunction, and may give rise to a global cerebral hypoperfusion. It appears that these complications precede progressive loss of axons, which mechanisms are complex and should be linked to a loss of β2 adrenergic receptors on astrocytes of demyelinating lesions.