Neuro-amelioration of cinnamaldehyde in aluminum-induced Alzheimer's disease rat model.

Hesham N Mustafa

Overview

Aluminum (Al) is a neurotoxic substance which has played an important role in the etiology, pathogenesis, and development of amyloid-? (A?) plaques. This study was carried out to evaluate the neuroprotective effect of aqueous cinnamon extract against aluminum chloride (AlCl3)-induced Alzheimer's disease. Forty adult male albino rats, randomly divided into four equal groups. Control group; ACE200 group administered aqueous cinnamon extract (ACE) orally; AlCl3 group received daily intraperitoneal (i.p.) injection of AlCl3 for 60 days to induce neurotoxicity and AlCl3 + ACE200 group received a combination of AlCl3 and ACE in the same dose and route as previous groups. Aluminum administration significantly enhanced the memory impairment and the A? formation in the rat model. The cerebellum exhibited a significant reduced number of Purkinje cells, marked decrease in the density of dendritic arborization and prominent perineuronal spaces in the molecular layer. There was loss of dendritic spines, neurofibrillary degeneration, and appearance of neuritic plaques. Concomitant administration of AlCl3 and ACE displayed an observable protection against these changes with progressive improvement in memory and intellectual performance. In conclusion, ACE may play a protective role against formation of amyloid-? plaques in cerebellum. KEYWORDS: Alzheimer; aluminum chloride; amyloid beta; apoptosis; cinnamon; memory

Summary

Aluminum (Al) is a neurotoxic substance which has played an important role in the etiology, pathogenesis, and development of amyloid-? (A?) plaques. This study was carried out to evaluate the neuroprotective effect of aqueous cinnamon extract against aluminum chloride (AlCl3)-induced Alzheimer's disease. Forty adult male albino rats, randomly divided into four equal groups. Control group; ACE200 group administered aqueous cinnamon extract (ACE) orally; AlCl3 group received daily intraperitoneal (i.p.) injection of AlCl3 for 60 days to induce neurotoxicity and AlCl3 + ACE200 group received a combination of AlCl3 and ACE in the same dose and route as previous groups. Aluminum administration significantly enhanced the memory impairment and the A? formation in the rat model. The cerebellum exhibited a significant reduced number of Purkinje cells, marked decrease in the density of dendritic arborization and prominent perineuronal spaces in the molecular layer. There was loss of dendritic spines, neurofibrillary degeneration, and appearance of neuritic plaques. Concomitant administration of AlCl3 and ACE displayed an observable protection against these changes with progressive improvement in memory and intellectual performance. In conclusion, ACE may play a protective role against formation of amyloid-? plaques in cerebellum. KEYWORDS: Alzheimer; aluminum chloride; amyloid beta; apoptosis; cinnamon; memory

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Author Comments

Dr. Hesham N Mustafa, MD
Dr. Hesham N Mustafa, MD
King Abdulaziz University
Associate Professor
Cell Biology - Electron Microscopy
Jeddah, Western Region | Saudi Arabia
Aluminum (Al) is a neurotoxic substance which has played an important role in the etiology, pathogenesis, and development of amyloid-? (A?) plaques. This study was carried out to evaluate the neuroprotective effect of aqueous cinnamon extract against aluminum chloride (AlCl3)-induced Alzheimer's disease. Forty adult male albino rats, randomly divided into four equal groups. Control group; ACE200 group administered aqueous cinnamon extract (ACE) orally; AlCl3 group received daily intraperitoneal (i.p.) injection of AlCl3 for 60 days to induce neurotoxicity and AlCl3 + ACE200 group received a combination of AlCl3 and ACE in the same dose and route as previous groups. Aluminum administration significantly enhanced the memory impairment and the A? formation in the rat model. The cerebellum exhibited a significant reduced number of Purkinje cells, marked decrease in the density of dendritic arborization and prominent perineuronal spaces in the molecular layer. There was loss of dendritic spines, neurofibrillary degeneration, and appearance of neuritic plaques. Concomitant administration of AlCl3 and ACE displayed an observable protection against these changes with progressive improvement in memory and intellectual performance. In conclusion, ACE may play a protective role against formation of amyloid-? plaques in cerebellum. KEYWORDS: Alzheimer; aluminum chloride; amyloid beta; apoptosis; cinnamon; memoryDr. Hesham N Mustafa, MD

Resources

https://www.ncbi.nlm.nih.gov/pubmed/31460853
https://www.ncbi.nlm.nih.gov/pubmed/31460853

Neuro-amelioration of cinnamaldehyde in aluminum-induced Alzheimer's disease rat model.

Authors:
Dr. Hesham N Mustafa, MD
Dr. Hesham N Mustafa, MD
King Abdulaziz University
Associate Professor
Cell Biology - Electron Microscopy
Jeddah, Western Region | Saudi Arabia
Dr. Mustafa H N, MD
Dr. Mustafa H N, MD
Anatomy Department, Faculty of Medicine, King Abdulaziz University, Jeddah, Kingdom of Saudi Arabia.
Associate Professor
Macroscopic and Microscopic Histology
Jeddah, Jeddah | Saudi Arabia

J Histotechnol 2020 03 28;43(1):11-20. Epub 2019 Aug 28.

Anatomy Department, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia.

Aluminum (Al) is a neurotoxic substance which has played an important role in the etiology, pathogenesis, and development of amyloid-? (A?) plaques. This study was carried out to evaluate the neuroprotective effect of aqueous cinnamon extract against aluminum chloride (AlCl)-induced Alzheimer's disease. Forty adult male albino rats, randomly divided into four equal groups. Control group; ACE200 group administered aqueous cinnamon extract (ACE) orally; AlCl group received daily intraperitoneal (i.p.) injection of AlCl for 60 days to induce neurotoxicity and AlCl + ACE200 group received a combination of AlCl and ACE in the same dose and route as previous groups. Aluminum administration significantly enhanced the memory impairment and the A? formation in the rat model. The cerebellum exhibited a significant reduced number of Purkinje cells, marked decrease in the density of dendritic arborization and prominent perineuronal spaces in the molecular layer. There was loss of dendritic spines, neurofibrillary degeneration, and appearance of neuritic plaques. Concomitant administration of AlCl and ACE displayed an observable protection against these changes with progressive improvement in memory and intellectual performance. In conclusion, ACE may play a protective role against formation of amyloid-? plaques in cerebellum.

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http://dx.doi.org/10.1080/01478885.2019.1652994DOI Listing
March 2020
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Suvarna KS et al.
2019

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