Fibroblast Growth Factor 21 and Autophagy Modulation Ameliorates Amyloid β-Induced Alzheimer Disease Pathology in Rats

Abstract

Alzheimer's disease (AD) is a multifactorial neurodegenerative condition and the most common cause of its initiation is accumulation of oligomeric amyloid beta1-42 (Aβ1-42). In recent past, several studies have shown autophagy deficits in AD may resulted accumulation of misfolded protein, Aβ1-42 and phosphorylated tau (ptau). Fibroblast growth factor 21 (FGF21), a metabolic hormone, has shown strong neuroprotective efficacy via increasing autophagic flux in AD. Therefore, this study was designed to investigate the synergistic neuroprotective efficacy of lentiviral FGF21 gene (LV-FGF21) delivery and rapamycin-autophagy modulator in Aβ1-42 induced AD in rats.