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Regul Toxicol Pharmacol. 2016 Jul;78:53-8. doi: 10.1016/j.yrtph.2016.04.006. Epub 2016 Apr 22.

Cereboost™, an American ginseng extract, improves cognitive function via up-regulation of choline acetyltransferase expression and neuroprotection.

Author information

1
College of Veterinary Medicine, Chungbuk National University, Cheongju, Chungbuk 28644, South Korea.
2
Anydoctor Healthcare Co., Ltd., Cheonan, Chungnam 31066, South Korea.
3
College of Veterinary Medicine, Chonnam National University, Gwangju 61186, South Korea.
4
College of Veterinary Medicine, Chungbuk National University, Cheongju, Chungbuk 28644, South Korea. Electronic address: yjm0000@hanmail.net.
5
College of Veterinary Medicine, Chungbuk National University, Cheongju, Chungbuk 28644, South Korea. Electronic address: solar93@cbu.ac.kr.

Abstract

In Alzheimer disease (AD), amyloid-beta (Aβ) peptides induce the degeneration of presynaptic cholinergic system, in which decreased activity of enzyme choline acetyltransferase (ChAT) responsible for acetylcholine synthesis is observed. Cereboost™, an extract of American ginseng extract, contains a high concentration of Rb1 ginsenoside which is a well-known ingredient improving human cognitive function. We investigated the effects of Cereboost™ on learning and memory function of mice challenged with an Aβ1-42 peptide and the underlying mechanisms in vitro. Cereboost™ protected against Aβ1-42-induced cytotoxicity in F3.ChAT stem cells, and enhanced the ChAT gene expression. Aβ1-42 injection into the mouse brain impaired the cognitive function, which was recovered by oral administration of Cereboost™. In addition, Cereboost™ restored brain microtubule-associated protein 2 and synaptophysin as well as acetylcholine concentration. The results demonstrate that Cereboost™ administration recovered the cognitive function of AD model animals by enhancing acetylcholine level via ChAT gene expression and neuroprotection.

KEYWORDS:

American ginseng (Panax quinquefolius); Amyloid-beta peptide; Cereboost™; Choline acetyltransferase; Cognitive function; Neuroprotection

PMID:
27112419
DOI:
10.1016/j.yrtph.2016.04.006
[Indexed for MEDLINE]

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