LAUSR

Alzheimer's disease (AD) is a neuronal dementia with progressive memory loss. Amyloid-beta (Aβ) peptides has major effect in the neurodegenerative disorder, which are thought to promote mitochondrial dysfunction in AD brains. Anti-AD drugs acting upon the brain are generally difficult to develop, often cause serious side effects or lack therapeutic efficacy. Numerous studies have shown the beneficial therapeutic applications of gold nanoparticles (AuNPs), including for neuroprotective events and AD. The aim of this study is to understand how AuNPs could exert their neuroprotective role in AD, for which cell model have chosen human neural stem cells (hNSCs) as the experimental tool. We hypothesize AuNPs protect against Aβ-induced cellular impairment and mitochondrial dysfunction in hNSCs. Here, we show AuNPs increase the survival of hNSCs treated with Aβ via downregulation of caspase 3 and 9 activities. Moreover, AuNPs abrogated the Aβ-mediated decrease neuroprotective (CREB and Bcl-2) and mitochondrial (PGC1α, NRF-1and Tfam) gene expressions in treated hNSCs. Importantly, co-treatment with AuNPs significantly rescued hNSCs from Aβ-mediated mitochondrial function and morphology. AuNPs also significantly normalizes the immunostaining of mitochondrial marker and mass in differentiated hNSCs with Aβ. The effects may be exerted by the AuNPs, as supported by its protective reversal of Aβ-induced cellular impairment and mitochondrial dysfunction in hNSCs. In fact, the results presented extend our understanding of the mechanisms through which AuNPs could exert their neuroprotective role in hNSCs treated with Aβ.