4.7 Article

Differential neuroprotective effect of curcuminoid formulations in aluminum chloride-induced Alzheimer's disease

Journal

ENVIRONMENTAL SCIENCE AND POLLUTION RESEARCH
Volume 29, Issue 45, Pages 67981-67996

Publisher

SPRINGER HEIDELBERG
DOI: 10.1007/s11356-022-20593-4

Keywords

Aluminum chloride; Anti-Alzheimer activity; Curcuma longa; Curcuminoid-rich extract; Neuroinflammation

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This study investigated the potential efficacy of curcuminoid-rich extract (CRE) and its ternary complex (TC) in the treatment of Alzheimer's disease (AD). The results showed that CRE and TC significantly improved behavioral and biochemical parameters, as well as acetylcholinesterase inhibitory activity. Histological analysis indicated that these supplements stabilized neurodegenerative changes and neuronal loss. Furthermore, CRE and TC supplementation downregulated the expression of pathological genes associated with AD. These findings suggest that CRE and TC may act as promising candidates for the prevention of AD through multiple underlying signaling pathways.
Alzheimer's disease (AD) is a slowly progressive brain degenerative disorder which gradually impairs memory, thinking, and ability to perform easy routine tasks. This degenerative disorder mainly targets the elderly people and has imposed an endemic burden on society. Hence, there is a crucial need to investigate the efficacious herbal pharmacotherapies that can effectively mitigate and prevent the pathological hallmarks of AD. The current study aims to explore the potential efficacy of curcuminoid-rich extract (CRE) and its ternary complex (TC). Experimental rodents were administered with AlCl3 (300 mg/kg) to induce AD and treated with rivastigmine, curcuminoid crude extract, CRE, and TC orally for three consecutive weeks. Neurobehavioral, biochemical, and histopathological studies were performed from the last week of the study period. The mRNA expression of different pathological biomarkers was estimated by RT-qPCR analysis. The results of the study suggested that CRE and TC significantly improved the behavioral, biochemical parameters and acetylcholinesterase inhibitory activity in treatment groups. Histological analysis was also carried out indicating that the neurodegenerative changes and neuronal loss were stabilized by CRE and TC supplementation. CRE and TC supplementation remarkably downregulated the interleukin-1 alpha, tumor necrosis factor-alpha, interleukin-1 beta, acetylcholinesterase, and beta-secretase pathological gene expression. Hence, it was concluded that CRE and TC may act as promising candidates in the prevention of AD via numerous underlying signaling pathways.

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