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Wu, Melissa P.

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Wu

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Melissa P.

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Wu, Melissa P.

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2013 - 20152

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Author's Publications: search.filters.isAuthorOfPublication.54a9fb15-f055-4f76-a01c-0cb3e71dbf88

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    Low-level light in combination with metabolic modulators for effective therapy of injured brain
    (Nature Publishing Group, 2015) Dong, Tingting; Zhang, Qi; Hamblin, Michael; Wu, Melissa P.
    Stem cell technology has facilitated the development of human cell culture models of disease that can be used to study pathogenesis and test therapeutic candidates. These models hold particular promise for complex neurological diseases such as Alzheimer’s disease (AD) because existing animal models have been unable to fully recapitulate all aspects of pathology. We recently reported the design and characterization of a novel three-dimensional (3D) culture system that exhibits key events in the pathogenic cascade of AD, including extracellular aggregation of amyloid β peptides and accumulation of hyperphosphorylated/aggregated tau protein. Here we provide instructions for the generation and analysis of 3D human neural cell cultures, including the production of genetically modified human neural progenitor cells (hNPCs) with familial AD (FAD) mutations, the differentiation of the hNPCs in a 3D Matrigel matrix, and the analysis of AD pathologenesis in this model. The same principles may be applicable to models of other inherited neurodegenerative diseases characterized by the aberrant aggregation of misfolded proteins.
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    Enhancing Myoblast Fusion for Therapy of Muscular Dystrophies
    (2013-10-08) Wu, Melissa P.; Gussoni, Emanuela; Wagers, Amy; Beggs, Alan; Girgenrath, Mahasweta; Dominov, Janice
    Skeletal muscle is a major organ comprising 30-40% of the human body mass. The coordination of processes resulting in mature muscle requires many genes, and their loss can result in debilitating muscle disorders. Of the strategies being developed to cure muscle diseases, enhancement of the natural process of muscle cell fusion in existing or introduced myogenic cells has great therapeutic potential. In this work, we determined whether a drug that stimulates proliferation and fusion of myoblasts could alleviate murine Duchenne muscular dystrophy. We also studied the necessity of a gene that is upregulated in early fusing human myoblast cultures and its role in muscle disease development.