Centella asiatica (L.) as a Neuroprotective agent in Alzheimer's Disease: A Focus on Mitochondrial Bioenergetics and Antioxidant Pathways

Alzheimer's disease is a progressive neurodegenerative disorder marked by cognitive decline, amyloid-beta accumulation, tau hyperphosphorylation, and chronic oxidative stress. Emerging evidence highlights mitochondrial dysfunction and impaired bioenergetics as central contributors to Alzheimer's disease pathogenesis. Centella asiatica a medicinal herb widely used in traditional systems of medicine, has demonstrated promising neuroprotective properties through its rich phytochemical profile, particularly triterpenoids such as asiaticoside and madecassoside. This review systematically explores the role of Centella asiatica in modulating mitochondrial bioenergetics and antioxidant pathways in the context of Alzheimer's disease. Centella asiatica enhances mitochondrial function by upregulating ATP synthesis, preserving mitochondrial membrane potential, and promoting biogenesis via PGC-1α activation. Concurrently, it activates the Nrf2 signalling pathway, leading to increased expression of endogenous antioxidant enzymes, including superoxide dismutase, catalase, and glutathione peroxidase. These mechanisms collectively reduce reactive oxygen species (ROS), mitigate lipid peroxidation, and prevent neuronal apoptosis. Preclinical studies support Centella asiatica's efficacy in improving cognitive performance, reducing neuroinflammation, and protecting against neurotoxicity. Although clinical data remain limited, the safety profile and multi-targeted action of Centella asiatica position it as a promising candidate for adjunctive therapy in Alzheimer's disease. Further translational research and clinical trials are warranted to validate its therapeutic potential and optimise its pharmacological application.