Gangarde_2025_J.Trace.Elem.Med.Biol_88_127612

BACKGROUND & AIMS: Cuscuta reflexa (family Convolvulaceae), commonly known as giant dodder or Amarbel, is a parasitic plant that has garnered attention in pharmacological research due to its diverse bioactive compounds and potential therapeutic applications. Scientific studies have validated its traditional uses in folk medicine, highlighting its pharmacological activities. Alzheimer's Disease (AD) is a neurodegenerative disorder marked by the buildup of amyloid-beta (Abeta) plaques and neurofibrillary tangles (NFT) in the brain, leading to synaptic impairment and the gradual loss of neurons. Currently, no effective medication is available to treat the development and progression of the disease. Hence, there is a rising concern about using alternative therapy such as herbal medicine to limit the progression of AD and improve the quality of a patient's life with minimum side effects. The plant Cuscuta reflexa has traditionally been claimed to possess neuroprotective effects but has not yet been validated scientifically. The present study aimed to investigate the potential of the hydroalcoholic extract of Cuscuta reflexa (CRE) to ameliorate the neurodegenerative effect of aluminium chloride (AlCl(3)) using in vitro and in vivo studies. METHODS: The neuroprotective activity of CRE was evaluated using in vitro and in vivo experimental models of AlCl(3)-induced AD. RESULTS: The in vitro study showed that CRE markedly reduced AlCl(3)-induced cytotoxicity in PC12 cells. The in vivo study using the AlCl(3)-induced AD rat model showed that CRE treatment improved learning and memory, as evaluated using the open field test (OFT) and Morris water maze (MWM) test. CRE also showed the reduction in oxidative stress induced by AlCl(3) in the brains of the rats by virtue of the significant decrease in oxidative stress biomarker malondialdehyde (MDA) and increase in the antioxidant parameters such as reduced glutathione (GSH), catalase (CAT) and superoxide dismutase (SOD). Further, CRE exhibited its cholinergic activity by lowering the AlCl(3)-induced enhanced levels of acetylcholinesterase (AChE) in the brains of rats. Histopathological analysis of the brains of rats showed that CRE treatment prevented the reactive changes and the damage in the neuronal tissue caused due to the AlCl(3). CONCLUSION: Conclusively, CRE ameliorated AlCl(3)-induced neurobehavioural toxicity in the rat model of AD by virtue of its anti-inflammatory, antioxidant, cholinergic and neuroprotective effects which suggests its use in the treatment of progressive neural damage and cognitive deficits in AD patients.