Mardani Abdul Halim1*, Nurlina Rosli2, Shaharum Shamsuddin3, Nazalan Najimudin2, Ghows Azzam2
1. Biotechnology Research Institute, Universiti Malaysia Sabah, Jalan UMS, 88400 Kota Kinabalu, Sabah, Malaysia
2. School of Biological Sciences, Universiti Sains Malaysia, 11800 Gelugor, Penang, Malaysia
3. School of Health Sciences, Universiti Sains Malaysia, 16150 Kubang Kerian, Kelantan, Malaysia
*Corresponding author: Mardani Abdul Halim.
ABSTRACT
INTRODUCTION: Alzheimer’s disease (AD) is a progressive neurodegenerative disorder marked by the accumulation of amyloid-beta (Aβ) plaques in the brain, leading to cognitive decline and functional impairment. It is among the most common and debilitating age-related conditions, with no definitive cure. Withania somnifera (Ashwagandha), a key herb in Ayurvedic medicine, is known for its adaptogenic and neuroprotective properties. Bioactive compounds in Ashwagandha have shown therapeutic potential in neurodegenerative diseases, including AD. However, in vivo experimental evidence, especially using genetic models of AD, remains limited and warrants further investigation.
OBJECTIVE(S): This study evaluated the neuroprotective effects of Withania somnifera in a Drosophila Alzheimer’s model by assessing its ability to reduce amyloid-beta toxicity, improve the rough eye phenotype, and enhance lifespan in both AD and wild-type flies.
MATERIALS & METHODS: In this study, Drosophila melanogaster was used as an in vivo model to investigate the therapeutic potential of Withania somnifera (Ashwagandha) in Alzheimer’s disease (AD). A transgenic Drosophila line expressing human amyloid-beta (Aβ) peptides in the eye tissue was employed to model AD-related neurodegeneration, while wild-type flies served as controls. Flies were reared on standard cornmeal-based food, with the treatment group receiving supplementation of Ashwagandha root powder at a concentration of 20 mg/mL. The rough eye phenotype (REP) was evaluated using stereomicroscopy to assess the extent of phenotypic rescue. To evaluate the effects on lifespan, both the AD model and wild-type flies were monitored daily, and survival rates were recorded to determine changes in longevity associated with Ashwagandha treatment.
RESULTS: The administration of 20 mg/mL Ashwagandha root powder led to a noticeable phenotypic improvement in the AD model flies, significantly rescuing the rough eye phenotype. This suggests a neuroprotective effect of Ashwagandha against amyloid-beta-induced damage in the Drosophila eye tissue. Additionally, a statistically significant increase in lifespan was observed in both the AD model flies and the WT flies treated with Ashwagandha, compared to untreated controls. These findings indicate that Ashwagandha may not only mitigate AD pathology but also promote general longevity and cellular well-being.
CONCLUSION: This study shows that Ashwagandha root powder improves neurodegeneration and extends lifespan in a Drosophila Alzheimer’s model. It significantly rescues the rough eye phenotype and enhances longevity in both AD and wild-type flies, indicating its therapeutic potential for Alzheimer’s and neural health. Further validation in mammalian models is needed.
KEYWORDS: Alzheimer’s Disease, Drosophila melanogaster, Longevity, Withania somnifera
