The unique molecular signature of cortical tissue injury in Multiple Sclerosis. Homo sapiens

In the present study we addressed several questions related to the mechanisms of cortical injury. We analyzed genome wide gene expression by microarrays, comparing active multiple sclerosis lesions with highly inflammatory lesions of chronic tuberculous meningitis, with neurodegenerative lesions of Alzheimer’s disease and with normal cortex of age matched controls. Overall design: To clarify which inflammatory mediators drive demyelination in the human cortex, we characterized and compared the gene expression profile of cortices derived from patients with progressive Multiple Sclerosis (MS), Meningitis tuberculosis (TB), Alzheimer's disease (AD) as well as of normal cortex from age matched controls (CO). 3 cases of each disease were included into the study. Preceding the gene expression profiling, all cases were characterized histologically and areas of interest were identified. RNA was isolated from those areas, amplified and hybridized to Agilent G4112A whole genome microarrays.