Elucidating the role of inflammatory processes in Alzheimer's disease pathophysiology using novel transgenic modeling
Our laboratory is interested in assessing the contribution of inflammation in the pathophysiology of Alzheimer's disease (AD). Inflammation has long been hypothesized to play a critical role in AD. Extant data support a more secondary role for inflammation in AD pathogenesis rather than an etiological one, however direct assessment of the latter has been lacking. We are utilizing novel transgenic models that separately harbor silent transgenes encoding potent inflammatory cytokines/chemokines, which will be expressed only when experimentally activated. These cytokines/chemokines were selected based upon their purported role(s) in brain inflammation and neurodegeneration with each exhibiting varying effects on the inflammatory cell milieu in the brain.
Developing novel virus vector-based therapies for neurodegenerative diseases
Simultaneously, we are developing novel Herpes simplex virus (HSV) amplicon vector-based AD vaccines directed against the amyloid-beta peptide, a proteolytic fragment of amyloid precursor protein believed to play an important role in AD pathogenesis. In addition, we are creating other HSV amplicon vectors that are capable of expressing selected therapeutic transgenes for protracted periods of time, a quality that present vector iterations do not possess. It is anticipated that these improved vectors will be more appropriate for the development of gene-based therapies for neurodegenerative diseases, such as Parkinson's disease.
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