Protective role of fucoidan against cognitive deficits and redox imbalance in a scopolamine-induced Alzheimer’s disease model in rats

This study examined the neuroprotective impacts of fucoidan on behavioral performance and oxidative damage in an animal model with scopolamine-induced cognitive deficits. Male Wistar rats, aged 8 weeks, were administered scopolamine (2 mg/kg) for 10 days. Fucoidan (15-60 mg/kg) or donepezil (1 mg/kg) was administered prior to behavioral tests over three consecutive weeks. To assess memory and learning, all rats underwent the Morris water maze (MWM) task and the Novel Object Recognition (NOR) test. Following the tests, the hippocampi and prefrontal cortex (PFC) of the rats were collected to evaluate oxidative stress parameters across all treatment groups. A significant decrease in the mean Q₂ time was observed during the probe trial in the water maze task after scopolamine injection on the test day. Administration of fucoidan (15-60 mg/kg) or donepezil (1 mg/kg) notably improved cognitive dysfunction (p < 0.001). Biochemical analysis demonstrated a decline in protein carbonyl and malondialdehyde levels, along with an elevation in reduced glutathione and total antioxidant capacity in the fucoidan-treated rats (15-60 mg/kg). It is supposed that cholinergic dysfunction and oxidative stress are key contributors to cognitive deficits, and fucoidan may protect the hippocampus and prefrontal cortex by mitigating oxidative damage biomarkers.