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Our laboratory researches mechanisms of neurodegeneration and
abnormal growth. We are primarily interested in the contributions of
exposure (preventable) factors and aberrant gene expression in the
pathogenesis of neuronal cell death and inappropriate growth of neurites in
the pathogenesis of neurodegeneration. Our lab has three general areas of
investigation: 1) We investigate the mechanisms by which ethanol, oxidative
stress, and free radical injury cause apoptosis of neuronal cells. We are
also trying to develop strategies of neuronal rescue using information
obtained about the mechanisms of cell death. 2) We study the mechanisms by
which abnormal expression of neuronal thread protein (NTP) or nitric oxide
synthase 3 leads to neurodegeneration characterized by apoptosis and
abnormal proliferation of neuronal cell processes (neuritic sprouting) as
occur in brains with Alzheimer's disease (AD). An exciting recent discovery
was that ethanol exposure, oxidative stress, and increased free radical
production exacerbate the effects of NTP or NOS-3 over-expression in
neuronal cells. 3) We investigate molecular mechanisms of primary malignant
brain tumor invasion. Our research is focused on determining how
over-expression of the aspartyl asparaginyl beta hydroxylase (AAH) gene
promotes invasive growth of primary brain tumors. Our research program
utilizes a broad array of modern methodological approaches.
de la Monte, S.M., Ghanbari, K., Frey, W.H., Beheshti, I., Averback, P., Hauser, S.L., Ghanbari, H.A., and J.R. Wands. Characterization of the AD7c-NTP cDNA expression in Alzheimer's disease and measurement of a 41-kD protein in cerebrospinal fluid. J. Clin. Invest. 100:3093-3104, 1997. de la Monte, S.M., Ganju, N., Banerjee, K., Brown, N.V., Luong, T., and J.R. Wands. Partial rescue of ethanol-induced neuronal apoptosis by growth factor activation of phosphoinositol-3-kinase. Alcohol. Clin. Exp. Res., 24:716-726, 2000. |
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