Noni (Morinda citrifolia) and Neurodegeneration: Exploring its Role in Oxidative Stress, Neuroinflammation, and Cell Survival Pathways #MMPMID41389093
Goel F; Garg VK
Mol Neurobiol 2025[Dec]; 63 (1): 289 PMID41389093show ga
Neurodegenerative illnesses like Alzheimer's, Parkinson's, and Huntington's diseases are characterized by neuronal progressive loss, oxidative injury, neuroinflammation, and cell survival pathway disturbance. Noni (Morinda citrifolia), a multifarious plant with phytochemical content that includes iridoids, flavonoids, polyphenols, and alkaloids, is of particular interest as a candidate following the demonstration of neuroprotective activity. This review addresses the molecular mechanism of neuroprotection of noni on the basis of its ability to modulate oxidative stress, suppress neuroinflammation, and control cell survival pathways. Noni activates the Nrf2/ARE pathway, which results in enhanced endogenous antioxidant defense mechanisms such as SOD, CAT, and GPx, scavenging ROS. Additionally, it suppresses neuroinflammation by inhibiting the NF-kappaB pathway, which reduces the release of pro-inflammatory cytokines (TNF-alpha, IL-1beta, IL-6). Moreover, noni controls cell survival through the PI3K/Akt/mTOR and MAPK pathways, promoting neuronal resistance and anti-apoptosis. Preclinical evidence is strong in showing the efficacy of noni against neurodegeneration, but clinical evidence is needed to ascertain its translational potential. However, despite promising preclinical evidence highlighting noni's neuroprotective potential, a significant gap remains in its clinical validation underscoring the need for a comprehensive evaluation of current findings to guide future translational research. This article stresses the multifaceted neuroprotective effects of noni and reasserts its therapeutic potential against neurodegenerative diseases.