{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,12,18]],"date-time":"2025-12-18T20:05:16Z","timestamp":1766088316464,"version":"3.41.2"},"reference-count":59,"publisher":"Oxford University Press (OUP)","issue":"4","license":[{"start":{"date-parts":[[2024,7,1]],"date-time":"2024-07-01T00:00:00Z","timestamp":1719792000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2024,7,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>The relationship between amyloid beta (A\u03b2) and oxidative stress (OS), both prominent factors in Alzheimer\u2019s disease-related neural degeneration, is deeply interconnected. The cleavage of the extracellular domain of Amyloid precursor protein (APP) and phosphorylating different substrates, respectively, the \u03b2-site amyloid precursor protein cleaving enzyme-1 (BACE-1) and Glycogen synthase kinase-3-beta (GSK-3\u03b2) enzymes initiate the synthesis of A\u03b2, which causes cognitive deficits in AD. This study aimed to explore the protective potential of Coenzyme Q10 (CoQ10). It also sought to uncover any synergistic effects when combined with donepezil, an acetylcholinesterase inhibitor, in treating Alzheimer\u2019s disease in male albino rats, focusing on the modulation of the BACE-1\/GSK-3\u03b2 pathway. The experiment involved 70 rats categorized into different groups: control, donepezil alone, CoQ10 alone, AD-model, donepezil co-treatment, CoQ10 co-treatment, and CoQ10\u00a0+\u00a0donepezil combination. Various assessments, such as cholinesterase activity, oxidative stress, serum iron profile, Brain Derived Neurotrophic Factor (BDNF), Tau protein, \u03b2-site amyloid precursor protein cleaving enzyme-1 (BACE-1), phosphatase and tensin homolog (Pten), and Glycogen synthase kinase-3-beta (GSK-3\u03b2), were conducted on behavioral and biochemical aspects. CoQ10 treatment demonstrated memory improvement, enhanced locomotion, and increased neuronal differentiation, mainly through the inhibition of the dual BACE-1\/GSK-3\u03b2. These findings were substantiated by histological and immunohistological examinations of the hippocampus.<\/jats:p>\n               <jats:p>Highlights Alzheimer\u2019s disease (AD) led to the alteration of BACE-1\/GSK-3\u03b2. Coenzyme Q10 (CoQ10) alleviated D-Gal and AlCl3-induced passive avoidance memory deficits in rats. CoQ10 counteracts Alzheimer\u2019s disease by inhibiting acetylcholine esterase. CoQ10 significantly increases levels of BDNF and diminishes Tau burden. CoQ10 acts as a dual BACE1\/GSK3\u03b2 inhibitor. The combination of CoQ10 treatment and donepezil demonstrated potential as a therapeutic approach.<\/jats:p>","DOI":"10.1093\/toxres\/tfae131","type":"journal-article","created":{"date-parts":[[2024,8,19]],"date-time":"2024-08-19T13:00:34Z","timestamp":1724072434000},"source":"Crossref","is-referenced-by-count":2,"title":["Anti-oxidant activity of coenzyme Q10 against AlCl3\/D-galactose in albino rat induced cognitive dysfunctions: Behavioral, biochemical, and BACE-1\/GSK-3\u03b2 alterations"],"prefix":"10.1093","volume":"13","author":[{"ORCID":"https:\/\/orcid.org\/0009-0002-2656-8668","authenticated-orcid":false,"given":"Nagat Fawzy","family":"Nawar","sequence":"first","affiliation":[{"name":"Division of Biochemistry , Department of Chemistry, Faculty of Science, , 31527 , Egypt"},{"name":"Tanta University , Department of Chemistry, Faculty of Science, , 31527 , 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