Neuroprotective Effects of Neolamarckia cadamba against β-amyloid-induced Cognitive Dysfunction via Antioxidant and Anti-inflammatory Mechanisms in Rats
Ravindra Mishra, Jeetendra Kumar GuptaIntroduction:
Alzheimer’s disease is a progressive neurodegenerative disorder characterised by oxidative stress, amyloid-beta accumulation, and neuroinflammation, leading to cognitive decline. Current treatments offer only limited symptomatic relief. This study evaluates the neuroprotective potential of the ethanolic leaf extract of Neolamarckia cadamba in an Aβ1-42-induced rat model of Alzheimer’s disease.
Methods:
Adult Wistar rats were divided into seven groups (n=6), and Alzheimer’s disease was induced by intracerebroventricular Aβ1-42 injection. Neolamarckia cadamba extract was administered orally for 21 days at doses of 100, 200, and 400 mg/kg. Cognitive and behavioural functions were evaluated using standard tests, while biochemical assays and ELISA assessed oxidative stress markers, antioxidant enzymes, and pro-inflammatory cytokines.
Results:
Aβ1-42 induction significantly impaired learning and memory and increased oxidative stress and inflammatory markers (p < 0.05). Treatment with Neolamarckia cadamba produced dose-dependent improvements, including reduced escape latency (up to 42% at 400 mg/kg, p < 0.01), improved behavioural performance, restoration of antioxidant enzymes (SOD, CAT, GSH), and reduced lipid peroxidation, nitric oxide, TNF-α, and IL-1β levels (p < 0.05), with the 400 mg/kg dose showing the greatest effect.
Discussion:
The observed effects of Neolamarckia cadamba may be attributed to its antioxidant, anti-inflammatory, and cholinergic modulatory properties, which contribute to the preservation of neuronal function and cognitive performance. Overall, the findings indicate dose-dependent improvements in both behavioural and biochemical parameters, supporting its potential neuroprotective role in the experimental model.
Conclusion:
The ethanolic extract of Neolamarckia cadamba demonstrated potential in attenuating Aβ1-42-induced cognitive impairments, possibly through antioxidant and anti-inflammatory mechanisms. These findings support its promise for further investigation in Alzheimer’s disease, with additional mechanistic and clinical studies required to establish its therapeutic applicability.