Effect of nabiximols oromucosal spray (Sativex) on symptoms associated with multiple sclerosis-related spasticity: a case series.

Spasticity and its related symptoms of spasms, pain, sleep disturbance and bladder dysfunction are common in persons with multiple sclerosis (MS) and may be interconnected through a common pathophysiology and/or may trigger and worsen each other. Tetrahydrocannabinol-cannabidiol (nabiximols) oromucosal spray (Sativex) is an add-on treatment for adults with moderate-to-severe MS spasticity who fail to respond adequately to conventional oral medications. There is evidence that nabiximols can ameliorate spasticity-associated symptoms irrespective of its effect on spasticity.

Glatiramer acetate increases phagocytic activity of human monocytes in vitro and in multiple sclerosis patients.

Beside its effects on T cells, a direct influence on cells of the myelo-monocytic lineage by GA becomes evident. Recently, we demonstrated that GA drives microglia to adopt properties of type II antigen presenting cells (APC) and increases their phagocytic activity. In the present work, we focused on human blood monocytes in order to examine whether GA may increase phagocytic activity in vivo and to evaluate the molecular mechanisms explaining this new discovered mode of action.

Glatiramer acetate modulates TNF-α and IL-10 secretion in microglia and promotes their phagocytic activity.

Glatiramer acetate (GA) is an approved immunomodulating agent for the treatment of relapsing-remitting multiple sclerosis. Its mode of action is attributed to a T helper cell-type 1 (Th1) to Th2 cytokine shift in T cells. Th2-type GA-reactive T cells migrate into the brain and act suppressive at the sites of inflammation.

Cortical demyelination is prominent in the murine cuprizone model and is strain-dependent.

The cuprizone model of toxic demyelination in the central nervous system is commonly used to investigate the pathobiology of remyelination in the corpus callosum. However, in human demyelinating diseases such as multiple sclerosis, recent evidence indicates a considerable amount of cortical demyelination in addition to white matter damage. Therefore, we have investigated cortical demyelination in the murine cuprizone model.