Neuroprotective Role of Echinochrome in Aluminium Chloride-induced Alzheimer's Disease in Rats

Alzheimer's Disease (AD) is the foremost neurodegenerative disorder and a variant of dementia observed in clinical environments. Echinochrome is a potent antioxidant and a natural bioproduct derived from sea urchins. The current study investigates the neuroprotective efficacy of echinochrome against aluminium chloride-induced AD in rats.

AD was induced using AlCl3 at a dosage of 200 mg/kg over a duration of four weeks, and the experimental design had four groups. The control group, AD group, and echinochrome were administered at 0.1 mg/kg and 1 mg/kg via intraperitoneal injection for 4 weeks.

The administration of echinochrome led to a decrease in escape latency time in the Morris maze, as well as reductions in malondialdehyde, nitric oxide, amyloid beta, tau protein, and acetylcholinesterase activity, while increasing levels of dopamine, serotonin, epinephrine, norepinephrine, glutathione, catalase, glutathione-S-transferase, and hippocampal histology. Moreover, echinochrome reinstates normal hippocampal histology, augmenting the number of pyramidal cells in the Cornuammonis area, as well as granular cells in the dentate gyrus region.

The administration of echinochrome to AD rats resulted in a reduction of escape latency time of the Morris maze, oxidative stress, amyloid beta, and Tau, while also restoring normal neurotransmitter levels and hippocampal histology.

Echinochrome exhibits neuroprotective properties against aluminium chloride-induced AD. The neuroprotective mechanisms of echinochrome include reducing oxidative stress, preventing the accumulation of amyloid beta and tau proteins, and suppressing acetylcholinesterase activity.