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Available4.4
16 reviewsAbstractBackground The deposition of toxic aggregated amyloid-β (Aβ), resulting from continuous cleavage of amyloid precursor protein (APP) by β-site APP cleaving enzyme 1 (BACE1) and γ-secretase, is a key pathogenic event in Alzheimer’s disease (AD). Small interfering RNAs (siRNA) have shown great potential for disease treatment by specifcally silencing target genes. However, the poor brain delivery efciency of siRNAs limits their therapeutic efcacy against AD.Methods We designed a simplifed and efective BACE1 siRNA (siBACE1) delivery system, namely, dendritic polyamidoamine modifed with the neurotropic virus-derived peptide RVG29 and polyethylene glycol (PPR@siBACE1).Results PPR@siBACE1 crossed the blood–brain barrier efciently and entered brain parenchyma in large amount, with subsequent neurotropism and potential microglia-targeting ability. Both in vitro and in vivo studies validated the efective brain delivery of siBACE1 and strong BACE1 silencing efciency. Treatment of AD mice with PPR@siBACE1 inhibited the production of Aβ, potentiated Aβ phagocytosis by microglia, improved the memory defcits and reduced neuroinfammatory response in AD mice.Conclusions This study provides a reliable delivery platform for gene therapies for AD.Keywords Microglia, Alzheimer’s disease, Nanomedicine, siRNA, Blood–brain barrier, BACE1, Aβ, Neuroinfammation
4.5
13 reviews