Abstract

Patients with multiple sclerosis (MS) often suffer from cognitive dysfunction; the underlying mechanisms have not been fully elucidated. Recent studies suggest that MS leads to heightened synaptic transmission and plasticity in different brain areas, and therefore may contribute to the observed behavioral abnormalities. Recent findings demonstrate synaptic plasticity changes in MS, including evidence from animal models of experimental autoimmune encephalomyelitis and human MS patients.

Keywords: Experimental autoimmune encephalomyelitis, inflammation, multiple sclerosis, N-methyl-D-aspartic acid, synaptic plasticity, trophic factor.