Advanced International Journal for Research

E-ISSN: 3048-7641     Impact Factor: 9.11

A Widely Indexed Open Access Peer Reviewed Multidisciplinary Bi-monthly Scholarly International Journal

Call for Paper Volume 7, Issue 2 (March-April 2026) Submit your research before last 3 days of April to publish your research paper in the issue of March-April.

Neuroprotective Role of Thymoquinone in Alzheimer's Disease Models: Mechanisms and Drug Design Perspectives

Author(s) Ms. Bhakti Vijaykumar Awalekar, Prof. Chandani Kamble
Country India
Abstract Abstract
Alzheimer's disease (AD) is a progressive neurodegenerative disorder that affects millions of people worldwide and is one of the leading causes of dementia in the elderly. It is mainly characterized by memory loss, behavioral changes, and a steady decline in cognitive functions. The underlying causes of AD are complex and involve multiple biological pathways such as oxidative stress, chronic inflammation, accumulation of amyloid-beta (Aß) plaques, tau protein tangles, mitochondrial dysfunction, and neuronal apoptosis. Because current treatments only provide symptomatic relief without effectively halting disease progression, there is an urgent need for novel, multi-targeted therapeutic agents .Thymoquinone (TQ), the main bioactive compound derived from the seeds of Nigella sativa (commonly known as black cumin),has emerged as a promising natural molecule with strong neuroprotective potential. TQ possesses potent antioxidant, anti-inflammatory, and anti-apoptotic properties that make it highly valuable in neurodegenerative research. Its antioxidant effect comes from its ability to neutralize reactive oxygen species (ROS) and enhance the activity of endogenous antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx). Through these mechanisms, TQ helps to maintain redox balance and prevent brain cells. In addition, TQ exhibits significant anti-inflammatory effects by reducing pro-inflammatory mediators such as tumor necrosis factor-alpha (TNF-a), interleukin-1ß (IL-1ß), and cyclooxygenase-2 (COX-2). By suppressing these inflammatory pathways ,TQ protects neurons from damage caused by chronic neuroinflammation - one of the key contributors to AD pathology. Experimental studies have also shown that TQ inhibits the aggregation of amyloid-beta peptides, reduces acetylcholinesterase activity, and improves cholinergic transmission, leading to
Keywords Keywords Nigella sativa (black cumin), Thymoquinone (TQ),Neurodegenerative disorder, Alzheimer's disease (AD), Computer Aided Drug Design, Molecular Docking .Chronic inflammation, Amyloid-beta (Aß) plaques, Alzheimer's disease models.
Field Medical / Pharmacy
Published In Volume 7, Issue 2, March-April 2026
Published On 2026-03-18

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