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生育三烯酚富集物补充剂可调节 APPswe/PS1dE9 阿尔茨海默病小鼠模型大脑海马的基因表达。

Tocotrienol Rich Fraction Supplementation Modulate Brain Hippocampal Gene Expression in APPswe/PS1dE9 Alzheimer's Disease Mouse Model.

机构信息

Department of Biochemistry, Faculty of Medicine, Universiti Kebangsaan Malaysia, Cheras, Kuala Lumpur, Malaysia.

Faculty of Medicine, Universiti Teknologi MARA, Sungai Buloh, Selangor, Malaysia.

出版信息

J Alzheimers Dis. 2019;70(s1):S239-S254. doi: 10.3233/JAD-180496.

DOI:10.3233/JAD-180496
PMID:30507571
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6700627/
Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by loss of memory and other cognitive abilities. AD is associated with aggregation of amyloid-β (Aβ) deposited in the hippocampal brain region. Our previous work has shown that tocotrienol rich fraction (TRF) supplementation was able to attenuate the blood oxidative status, improve behavior, and reduce fibrillary-type Aβ deposition in the hippocampus of an AD mouse model. In the present study, we investigate the effect of 6 months of TRF supplementation on transcriptome profile in the hippocampus of APPswe/PS1dE9 double transgenic mice. TRF supplementation can alleviate AD conditions by modulating several important genes in AD. Moreover, TRF supplementation attenuated the affected biological process and pathways that were upregulated in the AD mouse model. Our findings indicate that TRF supplementation can modulate hippocampal gene expression as well as biological processes that can potentially delay the progression of AD.

摘要

阿尔茨海默病（AD）是一种进行性神经退行性疾病，其特征是记忆力和其他认知能力丧失。AD 与海马脑区沉积的淀粉样β（Aβ）聚集有关。我们之前的工作表明，生育三烯酚丰富的部分（TRF）补充剂能够减轻血液氧化状态，改善行为，并减少 AD 小鼠模型中海马的纤维状 Aβ沉积。在本研究中，我们研究了 6 个月的 TRF 补充对 APPswe/PS1dE9 双转基因小鼠海马转录组谱的影响。TRF 补充可以通过调节 AD 中的几个重要基因来缓解 AD 状况。此外，TRF 补充还减弱了 AD 小鼠模型中上调的受影响的生物过程和途径。我们的研究结果表明，TRF 补充可以调节海马基因表达以及可能延缓 AD 进展的生物过程。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bf5/6700627/a8dd9856a6e0/jad-70-jad180496-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bf5/6700627/a9cf58d8fb6e/jad-70-jad180496-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bf5/6700627/744819263a56/jad-70-jad180496-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bf5/6700627/6379d206d238/jad-70-jad180496-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bf5/6700627/a9bcdee67a2b/jad-70-jad180496-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bf5/6700627/a8dd9856a6e0/jad-70-jad180496-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bf5/6700627/a9cf58d8fb6e/jad-70-jad180496-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bf5/6700627/744819263a56/jad-70-jad180496-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bf5/6700627/6379d206d238/jad-70-jad180496-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bf5/6700627/a9bcdee67a2b/jad-70-jad180496-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6bf5/6700627/a8dd9856a6e0/jad-70-jad180496-g005.jpg

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