Multiple sclerosis (MS)--autoimmune disease of CNS, characterized by myelin destruction and axonal damage. The action of drugs recommended for its treatment [symbol: see text] aimy[symbol: see text] at the reduction of the autoimmune responses. These responses lead to the neurological damage. One of immunoregulators is glatiramer acetate--Copaxone. Copaxone acts at different phases of MS pathogenesis and probably has a neuroprotective action. Copaxone reduces the rate of relapses and leads to clinical stabilisation in cases of relapsing-remmiting MS. Its efficacy and safety has been confirmed in long-term clinical and MRI-trials. Copaxone has few side-effects that are non-significant.

146 patients with multiple sclerosis are treated by copaxone in the Moscow MS Centre. The relaps exacerbation rate decreased by 72%, the relapse rate reduced by 25.6% during the copaxone treatment. EDSS score did not increase both in group with and without relapses. The condition of 2/3 patients was stable. To achieve the best effect of treatment the program of patient support was successfully used in the Moscow MS Centre.

Use of the "disease modifying" medicines is a significant success in multiple sclerosis (MS) treatment. These ways of MS treatment were scientificantly based and proved in large well-designed randomized studies, while direct mechanisms of their action is still under investigation. This review is discussing the mechanisms of action of glutiramer acetate (GA)--one of these medicines, modifying MS course. Its positive clinical effects in relapsing-remitting MS were shown in large clinical studies, confirmed by MRI and supported by extension trials. Immunomodulative effects of GA in MS and its experimental model (EAE) may be associated with induction of GA-specific cells clone, which have several positive for MS features, for example producing anti-inflammatory Th2-cytokines. Other characteristics of these cell clones should be studied further.

Results of the 2-year open postregistration study of Copaxone (glatiramer acetate), conducted in 3 Moscow leading medical centres are given. 32 MS patients with remitting-relapsing MS were investigated in accordance with international requirements (neurological scales, MRI of the brain, multimodal evoked potential). Significant reduction of annual relapse rate for 70.3%, stabilization of neurological status and benign safety profile were demonstrated during Copaxone treatment. Practical recommendations for Copaxone use are given.

Multiple sclerosis is universally accepted to be a multifactorial disease whose pathogenesis is due to a complex of immunopathological and pathochemical reactions. The key assumption is that only early stages of immunopathological chain reactions involve specific recognition of antigens by autoreactive T cells and antibodies. These early events trigger a demyelinating process at whose later stages of importance are macrophages and glial cells, particularly those of microglia, which produce a great deal of biologically active substances and inflammatory mediators. A deeper insight into the pathogenesis of multiple sclerosis has provided new therapeutical approaches to treating this disease. In addition to that there are effective IFN-beta drugs (Betaferon, Rebif, Avonex) and Copaxone, other pathogenetically justified approaches are still under search. The next step of further studies is to identify subtypes of multiple sclerosis and to choose a therapy in accordance with its pathogenetical mechanisms.

32 patients (21-55 years old) with multiple sclerosis (MS) were treated. Remittent form of the disease was observed in 24 patients, secondary progressive one--in 8 individuals; the degree of disability was characterised as scores 0-3 (the first group) and scores 5-6 (the second one) according to scale EDSS. Betaferon was administered subcutaneously in the dose of 8 MIU every other day during the period from several months to 1 year and more. Improvement of the state was observed in 5 patients with remittent form, stop of the development of disease (absence of either aggravations or signs of MS progression) was found in 26 cases (21 with remittent form, 4 with secondary progressive form). The conclusion was made: betaferon cannot cure but can stop progression of the disease. Indications and contraindications for betaferon therapy were established and recommendations were given concerning regimen of the treatment prophylaxis and therapy of side-effects.

The analysis of original and literature evidence on nimodipin administration in senile patients with vascular dementia and Alzheimer's disease allows the conclusion on positive effects of the drug on cognitive, motor, behavioral, neuropsychological and postural defects. Further efforts should be directed to the study of long-term regiments and elucidation of nimodipin ability to inhibit progression of dementia.

The analysis of original and literature evidence on nimodipin administration in senile patients with vascular dementia and Alzheimer's disease allows the conclusion on positive effects of the drug on cognitive, motor, behavioral, neuropsychological and postural defects. Further efforts should be directed to the study of long-term regimens and elucidation of nimodipin ability to inhibit progression of dementia.

As many as 50 patients aged over 60 years suffering from chronic vascular cerebral deficiency with equilibrium disorders are examined. The neurological- ly sharply defined symptomocomplexes explaining the equilibrium disorders and having stabilographic correlators are revealed in 2/3 of the cases. The subclinical patterns of postural instability in patients with various diseases are found in 1/3 of the cases. The stabilographic tests are performed as well as with the use of biologically reverse communication, resulting in rehabilitation measure in definite forms of the equilibrium disorder.

Leucine aminopeptidase of myelin was discovered to contain a protein subunit possessing, in contrast to the main enzymatic mass, antigenic properties and contained by different structures of the central nervous system. The protein was shown to be accumulated by neurons and astrocytes of embryonic tissue culture. The protein was absent from biological fluids of healthy persons and in schizophrenia but it was recordable in the blood and cerebrospinal fluid of patients with different forms of neurological pathology. In patients with neuronal degenerative diseases, the protein level in biological fluids in the terminal stages was significantly lower than in compensated patients.

Leucine aminopeptidase of myelin was discovered to contain a protein subunit possessing, in contrast to the main enzymatic mass, antigenic properties and contained by different structures of the central nervous system. The protein was shown to be accumulated by neurons and astrocytes of embryonic tissue culture. The protein was absent from biological fluids of healthy persons and in schizophrenia but it was recordable in the blood and cerebrospinal fluid of patients with different forms of neurological pathology. In patients with neuronal degenerative diseases, the protein level in biological fluids in the terminal stages was significantly lower than in compensated patients.