4.7 Article

Curcumin as a Potential Treatment for Alzheimer's Disease: A Study of the Effects of Curcumin on Hippocampal Expression of Glial Fibrillary Acidic Protein

期刊

AMERICAN JOURNAL OF CHINESE MEDICINE
卷 41, 期 1, 页码 59-70

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WORLD SCIENTIFIC PUBL CO PTE LTD
DOI: 10.1142/S0192415X13500055

关键词

Curcumin; Amyloid-B; Astrocyte; Glial Fibrillary Acidic Protein

资金

  1. National Natural Science Foundation of China [30770762]

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Curcumin, an agent traditionally utilized for its preventative action against tumorigenesis, oxidation, inflammation, apoptosis and hyperlipemia, has also been used in the treatment of Alzheimer's disease (AD). Recent advances in the study of AD have revealed astrocytes (AS) as being key factors in the early pathophysiological changes in AD. Glial fibrillary acidic protein (GFAP), a marker specific to AS, is markedly more manifest during morphological modifications and neural degeneration signature during the onset of AD. Several studies investigating the functionality of curcumin have shown that it not only inhibits amyloid sedimentation but also accelerates the disaggregation of amyloid plaque. Thus, we are interested in the relationship between curcumin and spatial memory in AD. In this study, we intend to investigate the effects of curcumin in amyloid-beta (A beta(1-40)) induced AD rat models on both the behavioral and molecular levels, that is to say, on their spatial memory and on the expression of GFAP in their hippocampi. Our results were statistically significant, showing that the spatial memory of AD rats improved following curcumin treatment (p < 0: 05), and that the expression of GFAP mRNA and the number of GFAP positive cells in the curcumin treated rats was decreased relative to the AD group rats (p < 0: 05). Furthermore, the expression level of GFAP mRNA in hippocampal AS in the AD rats significantly increased when compared with that in the sham control (p < 0: 05). Taken together, these results suggest that curcumin improves the spatial memory disorders (such disorders being symptomatic of AD) in A beta(1-40)-induced rats by down regulating GFAP expression and suppressing AS activity.

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