作者: S Gnanapavan
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摘要: The aim of this work was to investigate putative biomarkers neuronal plasticity and repair in the central nervous system. effects different disease processes, such as inflammation, demyelination neurodegeneration were explored. We developed validated ELISA-based assays for quantification neural cell adhesion molecule (NCAM) growth-associated protein (GAP)-43, two known facilitators outgrowth NCAM isoforms biological samples characterised using mass spectrometry. Soluble measured in-vitro in-vivo models inflammation/demyelination neurodegeneration, across neurological disorders CSF understand impact inflammation axonal loss on its levels. Recombinant GAP-43 produced baculovirus technology purified appreciable amounts use a new ELISA. levels quantified CSF. Values correlated with clinical outcome measures. demonstrated restricted pattern expression compared that serum whilst is almost exclusively expressed CSF, indicating these are intrathecally synthesised. lower prominent injury; multiple sclerosis, movement disorders, motor neurone disease, Alzheimer’s meningitis. In vitro culture model vivo experimental autoimmune encephalomyelitis studies demonstrate correlates well progression sclerosis. A similar relationship not found GAP-43. conclusion, adult CNS may possess intrinsic capacity repair, but be dramatically reduced states. Measuring process important understanding plasticity.