Green Coffee Bean Extract Mitigates Alzheimer's Disease in Male Rats.
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| Title: | Green Coffee Bean Extract Mitigates Alzheimer's Disease in Male Rats. |
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| Authors: | Abu-Almakarem, Amal S.1 (AUTHOR), R. Alzahrani, Othman2 (AUTHOR), Abu-Khudir, Rasha3,4 (AUTHOR), Alassar, S. R.5 (AUTHOR), El-Said, Karim Samy4 (AUTHOR) kareem.ali@science.tanta.edu.eg, Alkhodair, Sahar Abdulrahman6 (AUTHOR), Banjabi, Abeer A.6 (AUTHOR), Al-Bazi, Maha M.6,7 (AUTHOR), Mobasher, Maysa A.8 (AUTHOR), Soliman, Mohamed Mostafa9,10 (AUTHOR), Bose, Anupama (AUTHOR) abose@wiley.com |
| Source: | Journal of Food Biochemistry. 5/19/2026, Vol. 2026, p1-19. 19p. |
| Subjects: | Alzheimer's disease, Neuroprotective agents, Neurodegeneration, Oxidative stress, Plant extracts, Inflammation, Cognitive ability, PI3K/AKT pathway |
| Abstract: | Green coffee bean extract (GCBE) has shown potential for antioxidants and anti‐inflammation due to its rich composition of bioactive compounds and polyphenols that possess neuroprotective properties, which have been suggested to counteract neurodegenerative processes associated with Alzheimer's disease (AD). This study investigated the effect of GCBE treatment on aluminum chloride (AlCl3)‐induced AD in male rats. The pharmacokinetic properties of GCBE bioactive compounds were analyzed using the ADMET Lab 2.0 web servers, and molecular docking studies were performed using AutoDock Vina. Forty male Sprague–Dawley rats were divided into four equal groups; Group I was the negative control group; Group II received 250 mg/kg of GCBE (1/10 of LD50) from the 25th day to the 36th day; Group III was given AlCl3 (175 mg/kg) orally for 25 days, and Group IV was administered AlCl3 for 25 days, like in Group III, and then treated with GCBE as in Group II. The results indicated that GCBE demonstrated promising phytochemical constituents with safe pharmacokinetic profiles. The LD50 of GCBE was 2500 mg/kg b. wt. Behavioral assessments revealed significant improvement in cognitive performance in GCBE‐treated rats compared with the untreated AD group. Biochemical analyses demonstrated that GCBE significantly reduced oxidative stress and inflammatory markers. Moreover, GCBE markedly upregulated the expression of protein kinase (Akt1), cAMP‐response element binding protein (CREB), and brain‐derived neurotrophic factor (BDNF) indicating activation of neuroprotective signaling pathways. Histopathological examination further confirmed the protective effects of GCBE on hippocampal neuronal integrity. These findings suggest that GCBE exerted significant neuroprotective effects against AD, potentially through upregulation of the Akt/CREB/BDNF pathway, highlighting its potential as a promising therapeutic strategy for neurodegenerative disorders. [ABSTRACT FROM AUTHOR] |
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| Database: | Engineering Source |
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| Abstract: | Green coffee bean extract (GCBE) has shown potential for antioxidants and anti‐inflammation due to its rich composition of bioactive compounds and polyphenols that possess neuroprotective properties, which have been suggested to counteract neurodegenerative processes associated with Alzheimer's disease (AD). This study investigated the effect of GCBE treatment on aluminum chloride (AlCl3)‐induced AD in male rats. The pharmacokinetic properties of GCBE bioactive compounds were analyzed using the ADMET Lab 2.0 web servers, and molecular docking studies were performed using AutoDock Vina. Forty male Sprague–Dawley rats were divided into four equal groups; Group I was the negative control group; Group II received 250 mg/kg of GCBE (1/10 of LD50) from the 25th day to the 36th day; Group III was given AlCl3 (175 mg/kg) orally for 25 days, and Group IV was administered AlCl3 for 25 days, like in Group III, and then treated with GCBE as in Group II. The results indicated that GCBE demonstrated promising phytochemical constituents with safe pharmacokinetic profiles. The LD50 of GCBE was 2500 mg/kg b. wt. Behavioral assessments revealed significant improvement in cognitive performance in GCBE‐treated rats compared with the untreated AD group. Biochemical analyses demonstrated that GCBE significantly reduced oxidative stress and inflammatory markers. Moreover, GCBE markedly upregulated the expression of protein kinase (Akt1), cAMP‐response element binding protein (CREB), and brain‐derived neurotrophic factor (BDNF) indicating activation of neuroprotective signaling pathways. Histopathological examination further confirmed the protective effects of GCBE on hippocampal neuronal integrity. These findings suggest that GCBE exerted significant neuroprotective effects against AD, potentially through upregulation of the Akt/CREB/BDNF pathway, highlighting its potential as a promising therapeutic strategy for neurodegenerative disorders. [ABSTRACT FROM AUTHOR] |
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| ISSN: | 01458884 |
| DOI: | 10.1155/jfbc/5511502 |
