Brain Transduction

The brain is an attractive target for gene therapy to treat CNS structural and functional deficits such as aging-related memory loss, Parkinson's disease, Alzheimer's disease, or amyotrophic lateral sclerosis. Zou et al.[9] compared the efficiency, toxicity, and persistence of HDAd and FGAd vector-mediated gene transfer into the hippocampus or lateral ventricle of the brain in 20-month-old rats. Transgene expression peaked 6 days postinjection for both vectors. In the hippocampus, transgene expression from the FGAd decreased rapidly after day 6, being significantly lower than HDAd-injected hippocampus by day 16, and undetectable by day 183. In the ventricle, transgene expression from FGAd was significantly lower than HDAd by day 33 and undetectable by day 66. In contrast, transgene expression from the HDAd remained relatively stable with expression remaining >60% of peak levels on day 183. Overall, expression from HDAd was significantly higher than from FGAd at all time points after 6 days. First-generation Ad vectors induced substantial inflammatory and immune response which were significantly higher than those induced by HDAd at all time points after 3 hr. While both vectors induced a rapid increase in the proinflammatory cytokine that peaked at 3 hr postinjection, by 3 days, the level was significantly lower in the HDAd-treated brains than the FGAd-treated brains.

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