Protective Effect of Crocin against Mitochondrial Damage and Memory Deficit Induced by Beta-amyloid in the Hippocampus of Rats

Alzheimer’s disease is the most common form of dementia among the elderly. This progressive neurodegenerative disorder affects brain regions that control cognition, memory, language, speech, and awareness. As a potent antioxidant, crocin has been proposed to effectively manage the neurodegenerative disease. In this study, the recovery effects of crocin on the memory deficits caused by the intra-hippocampal injection of amyloid beta1-42 (Aβ1-42) were evaluated in rats. We also considered the protective effects of crocin on the mitochondrial damage caused by Aβ1-42. We examined the memory deficits of rats with the help of the Morris water maze. Then, we determined different mitochondrial toxicity endpoints caused by Aβ1-42, including mitochondrial ROS formation, lipid peroxidation, mitochondrial membrane potential collapse, mitochondrial outer membrane integrity, and cytochrome c release. Our results demonstrated that the behavioral signs of memory deficiency caused by Aβ1-42 significantly (P < 0.01) reduced by both pretreatment and post-treatment with crocin (30 mg/kg). Furthermore, crocin prevented all the Aβ1-42 induced above referenced mitochondrial upstream toxic events leading to neuronal apoptosis. These results demonstrated that crocin is a promising preventive candidate for the potential treatment of Alzheimer’s disease. Furthermore, it seems that the antioxidant and neuroprotective effects of crocin are better seen when the compound is pretreated beforehand rather than introduced afterward in Aβ1-42 exposed mitochondria.