Neuroprotective effects of Akebia Quinata extract on cognitive impairment in rat models

• Author Details:   
• Namrata M. Waghmare ^*
• Vinay V. Sarode
• Pragati G. Zalwade
• Dhamsheela N. Gondane
• Aditi B. Daiwalkar
• Bhushan R. Gandhare

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Background and Aim: Alzheimer’s disease (AD) involves cognitive decline driven by cholinergic dysfunction, oxidative stress, and neuroinflammation. This study investigates the neuroprotective efficacy of Akebia quinata ethanolic extract (AQE) against scopolamine-induced Alzheimer's Disease (AD) in rats, emphasizing memory, biochemical markers, and histopathological outcomes.

Materials and Methods: Wistar rats were divided into five groups: normal control, scopolamine-induced AD control, rivastigmine (2.5 mg/kg), and AQE (200/400 mg/kg). AD was induced via scopolamine (1 mg/kg), followed by 14-day treatments. Behavioural assessments (Radial Arm Maze/RAM, Novel Object Recognition Test/NORT) evaluated memory. Biochemical parameters (acetylcholinesterase/AChE, reduced glutathione, catalase, malondialdehyde/MDA, nitric oxide/NO) and histopathological changes in brain tissue were analysed.

Results: AQE (400 mg/kg) significantly enhanced memory retention, reducing Radial Arm Maze (RAM) errors and increasing novel object exploration time in the Novel Object Recognition Test (NORT). Biochemically, AQE lowered AChE activity, MDA, and NO levels while elevating glutathione and catalase, indicating reduced oxidative stress. Histopathology revealed preserved neuronal architecture, diminished amyloid plaques, and fewer neurofibrillary tangles in AQE-treated groups, with 400 mg/kg showing near-normal histology.

Conclusion: Akebia quinata extract mitigates scopolamine-induced AD by restoring cholinergic function, suppressing oxidative damage, and attenuating neurodegeneration. The 400 mg/kg dose demonstrated rivastigmine-comparable efficacy, highlighting AQE’s potential as a herbal alternative for AD management. Its neurobiological activity, attributed to flavonoids, alkaloids, and polyphenols, positions AQE as a novel therapeutic candidate. Further studies are warranted to validate clinical applicability