Research reportβ-glucan attenuated scopolamine induced cognitive impairment via hippocampal acetylcholinesterase inhibition in rats

- In silico study revealed good affinity of β-glucan for active site of AChE enzyme.
- β-glucan inhibited the AChE enzyme in vitro (IC50=0.68±0.08 µg/µl).
- β-glucan significantly reversed Scopolamine induced amnesia in Morris water maze.
- β-glucan has no effect on locomotor activity.
- β-glucan treatment inhibited AChE enzyme in the hippocampus of rats.

β-glucan (polysaccharide) rich diet has been reported to enhance cognition in humans but the mechanism remained elusive. Keeping this in mind, the present study was designed to investigate the interaction of β-glucan with central cholinergic system. Briefly, in-silico analysis revealed promising interactions of β-glucan with the catalytic residues of acetylcholinesterase (AChE) enzyme. In line with this outcome, the in vitro assay (Ellman's method) also exhibited inhibition of AChE by β-glucan (IC50=0.68±0.08 μg/µl). Furthermore, the in vivo study (Morris water maze) showed significant dose dependent reversal of the amnesic effect of scopolamine (2 mg/kg i.p.) by β-glucan treatment (5, 25, 50 and 100 mg/kg, i.p.). Finally, the hippocampi of aforementioned treated animals also revealed dose dependent inhibition of AChE enzyme. Hence, it can be deduced that β-glucan possesses potential to enhance central cholinergic tone via inhibiting AChE enzyme. In conclusion, the present study provides mechanistic insight to the cognition enhancing potential of β-glucan. Keeping in mind its dietary use and abundance in nature, it can be considered as economic therapeutic option against cognitive ailments associated with decline in cholinergic neurotransmission.

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