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Given the participation of amyloid beta (Aβ) in Alzheimer's disease (AD) pathogenesis the derivation of experimental therapeutics to prevent Aβ fibrillogenesis and/or enhance removal of parenchymal amyloid deposits represent viable disease-modifying approaches. Active Aβ-based immunotherapies have shown promise in mouse AD models, but application in human trials was accompanied by moderate brain inflammation...
The development and implementation of direct gene transfer technologies for the study and treatment of chronic CNS disorders inherently requires consideration of vector safety. Virus-based vectors represent the most efficient modalities but harbor the potential to induce vigorous innate and adaptive immune responses when administered in vivo. These responses can arise because of virus particle components,...
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