Neuroprotective effects of magnolol in aluminium chloride and D-galactose induced Alzheimer’s disease model

Abhinav Anand Navneet Khurana Neha Sharma Rajesh Kumar Daisy Sharma Neelam Kumari Bhupendra Singh   

Open Access   

Published:  Feb 17, 2026

DOI: 10.7324/JAPS.2026.289886
Abstract

Alzheimer’s disease (AD) is a disorder associated with continuing deterioration of neurons in the brain and is characterised by aggregation of neurotoxic amyloid beta (Aβ) plaques. It is also accompanied by increased oxidative stress, cholinergic impairment, and remarkably reduced brain-derived neurotrophic factor (BDNF). The net result is progressive loss of memory and cognitive abilities. The study aims to explore the anti-AD profile of magnolol. AD was induced in adult Swiss albino mice by simultaneously administering aluminium chloride at a dose of 5 mg/kg/ day; p.o. and D-galactose at a dose of 60 mg/kg/day; i.p. for a period of 90 days. The dose dependent ameliorative effect of magnolol (20 and 40 mg/kg/day; p.o.) was assessed with the help of behavioural, biochemical and Enzyme- Linked Immunosorbent Assay (ELISA) analyses. Magnolol was shown to ameliorate memory and cognitive insufficiencies as assessed from Morris Water Maze, Elevated Plus Maze and Novel Object Recognition paradigms. It also elicited a remarkable antioxidant effect, as evidenced by analysing various parameters like thiobarbituric acid reactive substances, glutathione, and catalase. Magnolol also had an inhibitory activity on acetylcholinesterase, β-secretase and caspase-3. Disintegration of Aβ plaques and improvement of BDNF levels were also reported in the present study. Magnolol presents a multifactorial approach, beyond its conventional antioxidant mechanism, against experimentally induced AD in mice.


Keyword:     Magnolol antioxidant phytoconstituent neuroprotective traditional


Citation:

Anand A, Khurana N, Sharma N, Kumar R, Sharma D, Kumari N, Singh B. Neuroprotective effects of magnolol in aluminium chloride and D-galactose induced Alzheimer’s disease model. J Appl Pharm Sci. 2026. Article in Press. http://doi.org/10.7324/JAPS.2026.289886

Copyright: © The Author(s). This is an open-access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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