Alzheimer's disease (AD) is a chronic, progressive, multifactorial, and the most common
neurodegenerative disease which causes
dementia and
mental deterioration in the elderly. The available treatments for AD are not disease-modifying drugs and only provide symptomatic relief.
Astaxanthin (ATX), a second-generation
antioxidant, is a dark red
carotenoid and exhibits the highest
antioxidant capacity, anti-inflammatory, neuroprotective, and antiapoptotic effects. In this study, we investigated the
therapeutic effect of different doses of ATX on the cerebral cortex and hippocampus of AD-like rats. The AD-like model was induced in rats using hydrated
aluminum chloride (
AlCl3.6H2O)
solution that was given orally at a dose of 75 mg/kg daily for 6 weeks. Morris water maze (MWM) behavioral test was performed to confirm the
cognitive dysfunction then AD-like rats were orally treated with different doses of ATX (5, 10, and 15 mg/kg) dissolved in
dimethyl sulfoxide (
DMSO) for six weeks. The results indicated that ATX significantly and dose-dependently improved the performance of AD-like rats treated with ATX during MWM and suppress the accumulation of
amyloid β1-42 and
malondialdehyde. Also, significantly inhibit
acetylcholinesterase and
monoamine oxidase activities and the expression of β-site
amyloid precursor
protein cleaving
enzyme 1 (BACE 1). ATX also significantly elevated the content of
acetylcholine,
serotonin, and nuclear factor erythroid-2-related factor 2 (Nrf2) and miRNA-124 expression. The effect of ATX treatment was confirmed by histopathological observations using H&E
stain and morphometric tissue analysis. From this study, we concluded that ATX may be a promising therapeutic agent for AD through targeting different pathogenic pathways.