Therapeutic potential of cedrol in alleviating cognitive impairments in aluminum chloride-induced Alzheimer's disease: A biomarker-based approach
Background: Alzheimer's disease (AD) is a progressive neurological disorder that impacts cognitive ability, characterized by amyloid plaques and neurofibrillary tangles. Cedrol is a bioactive sesquiterpene known for its health benefits and has been shown to reduce cellular dysfunction related t...
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| Main Authors: | , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Elsevier
2025-07-01
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| Series: | Results in Chemistry |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S2211715625004709 |
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| Summary: | Background: Alzheimer's disease (AD) is a progressive neurological disorder that impacts cognitive ability, characterized by amyloid plaques and neurofibrillary tangles. Cedrol is a bioactive sesquiterpene known for its health benefits and has been shown to reduce cellular dysfunction related to chronic conditions such as cardiovascular disease and cancer. Aluminum chloride (AlCl3), a prevalent environmental pollutant in food and drinking water, disrupts cerebral function, inducing oxidative stress, inflammatory responses, and cognitive decline, all of which are associated with the pathology of AD. Methodology: This study evaluated the anti-Alzheimer's properties of Cedrol by investigating its effects on free radical scavenging and its inhibitory efficacy against cholinesterases, specifically acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE). The study also assessed its impact on inflammatory enzymes such as lipoxygenase (LOX), tumor necrosis factor alpha (TNF-α), and cyclooxygenase-2 (COX-2), as well as additional enzymes, including glycogen synthase kinase-3 beta (GSK-3β), Rho-associated protein kinase II (ROCK II), and Na+/K+ ATPase. To evaluate oxidative stress, the levels of reduced glutathione, malondialdehyde, and nitric oxide, along with the activities of catalase and superoxide dismutase, were measured in male Wistar rats induced by AlCl3. Key findings: The study found that Cedrol improved cognitive impairment in a dose-dependent manner by reducing oxidative stress and enhancing cholinergic function. It also suppressed several AD biomarkers. In silico studies suggested that Cedrol's strong affinity for these biomarkers suggests its potential in regulating AD pathogenesis. Conclusion: Cedrol alleviated memory impairments and tissue damage produced by AlCl3 toxicity. |
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| ISSN: | 2211-7156 |