A Novel Curcumin-Based Formulation Offers Protection Against Neurodegeneration in Rat Models of AlCl3 Induced Alzheimer’s Disease

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 A Novel Curcumin-Based Formulation Offers Protection Against Neurodegeneration in Rat Models of AlCl3Induced Alzheimer’s Disease

Mohamed Arif1*, V. Gayathri2, Radhika Ravindran3,P. Kalaivani2, R. Siva2, Shonam Tamrakar2 1Gidaa Life Sciences Private Limited, 287, 9th Cross, Bapuji Layout Near Chandra Layout, Vijayanagara, Bangalore, Karnataka 560040, India. 2Centre for Toxicology and Developmental Research, Sri Ramachandra Institute of Higher Education and Research (Deemed to be University), No. 1, Ramachandra Nagar, Porur, Chennai 600116, Tamil Nadu, India. 3Tissue Engineering and Biomaterials Lab, Department of Biotechnology, IIT Madras, India. *Corresponding Author: Mohamed Arif, Gidaa Life Sciences Private Limited, 287, 9th Cross, Bapuji Layout Near Chandra Layout, Vijayanagara, Bangalore, Karnataka 560040, India. DOI: https://doi.org/10.58624/SVOANE.2026.07.030 Received: July 31, 2026 Published: August 18, 2026 Citation: Arif M, Gayathri V, Ravindran R, Kalaivani P, Siva R, Tamrakar S. A Novel Curcumin-Based Formulation Offers Protection Against Neurodegeneration in Rat Models of AlCl3-Induced Alzheimer’s Disease. SVOA Neurology 2026, 7:4, 220-238. doi.org/10.58624/SVOANE.2026.07.030 

 Abstract 

The exact mechanisms underlying Alzheimer’s disease (AD) pathogenesis are not fully understood, and effective disease-modifying treatments remain lacking despite decades of AD research. Therefore, alternative therapeutic approaches that may target multiple mechanisms of action underlying AD and have a better safety profile than synthetic drugs, such as phytotherapy, are being explored. We aimed to assess the neuroprotective properties of a novel curcumin formulation fortified with andrographolides and piperine (MAG XXI) in rat models of aluminium chloride–induced AD. Overall, 30 male Wistar rats were included and divided into five groups (a healthy control group, a non-treated AD group, and three AD groups treated with donepezil or 200/400 mg/kg body weight of MAG XXI). The Morris water maze, passive avoidance, and elevated plus maze tests were performed on the rats. Tissue samples from the cortex and hippocampus of the rats were then subjected to biochemical evaluation of neuronal, oxidative stress, and inflammatory markers. Compared to non-treated rats, donepezil-treated rats and high-dose (400 mg/kg body weight) MAG XXI–treated rats showed a mild but significant improvement in the Morris water maze and elevated plus maze test findings and a marked and significant improvement in the passive avoidance task results. Furthermore, oxidative stress markers, inflammatory markers, and neuronal markers improved overall in the donepezil-treated group and in both MAG XXI–treated groups. Notably, the improvement in the oxidative stress markers was more marked with MAG XXI (both doses) than with donepezil. Histopathological examination revealed lower incidence rates of neurofibrillary tangles, gliosis, and neuronal degeneration in the high-dose MAG XXI and donepezil groups. Notably, cresyl staining revealed minimal-to-mild cell dispersion in the donepezil group, whereas normal neuronal cells with well-lineated cell bodies and Nissl substance were observed in the high dose MAG XXI group. No adverse events were noted in the MAG XXI groups. MAG XXI could be a promising alternative for AD treatment because it appears to exhibit neuroprotective properties, as demonstrated by its ability to alleviate oxidative stress and neuroinflammation. However, further clinical trials involving humans are necessary to corroborate the present study’s results