MMP-2, VCAM-1 and NCAM-1 expression in the brain of rats with experimental autoimmune encephalomyelitis as a trigger mechanism for synaptic plasticity and pathology

Decreased NCAM-1 expression in CA1 and CA3 fields of the hippocampus, and in a lesser degree in the basal ganglia, limbic structure and cervical spinal cord, support the concept that the demyelinating neuroinflammatory damage in an autoimmune brain affect synaptic organization of the brain, altering the balance between extracellular proteases and cell adhesion molecules which appears to be critical for both the brain plasticity and autoimmune processes.