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用苹果酸铝处理老龄新西兰兔后基因组DNA稳定性的研究:与阿尔茨海默病动物模型的相关性。

Studies on genomic DNA stability in aluminium-maltolate treated aged new zealand rabbit: relevance to the alzheimers animal model.

作者信息

Magisetty Obulesu, Rao Dowlathabad Muralidhara, M Shama Sundar N

机构信息

Department of Anatomy, JSS Medical College, Mysore, India.

出版信息

J Clin Med Res. 2009 Oct;1(4):212-8. doi: 10.4021/jocmr2009.09.1265. Epub 2009 Oct 16.

DOI:10.4021/jocmr2009.09.1265
PMID:22461871
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3299183/
Abstract

BACKGROUND

Alzheimers disease (AD) is a devastative neurodegenerative disorder. Lack of substantial animal model that can unravel molecular underpinnings has been a major lacuna which limited the understanding of the etiology of the disease in turn limiting the employment of potential therapeutic strategies to combat the disease for a few decades. Our studies for the first time provided substantial animal model and tattered the etiology of the disease at a molecular level.

METHODS

In this study DNA was isolated from Hippocampus (H), Midbrain (M) and Frontal Cortex (Fc) of control and aluminium maltolate (Al-M) treated aged New Zealand rabbit brain. DNA damage has been studied using Agarose gel electrophoresis, Ethidium Bromide (EtBr) binding and Melting temperature techniques.

RESULTS

Al-M treated aged New Zealand rabbit's H and M showed higher DNA damage compared to corresponding controls, where as Fc showed mild DNA damage compared to corresponding controls.

CONCLUSIONS

This study tangibly provides substantial molecular level understanding of the disease in turn providing an adequate platform to streamline potential therapeutic strategies.

KEYWORDS

Alzheimer's disease; Aluminium maltolate; Animal model; DNA damage.

摘要

背景

阿尔茨海默病(AD)是一种毁灭性的神经退行性疾病。缺乏能够揭示分子基础的实质性动物模型一直是一个主要缺陷,这限制了对该疾病病因的理解,进而在几十年里限制了对抗该疾病的潜在治疗策略的应用。我们的研究首次提供了实质性的动物模型,并在分子水平上破解了该疾病的病因。

方法

在本研究中,从对照和经苹果酸铝(Al-M)处理的老年新西兰兔脑的海马体(H)、中脑(M)和额叶皮质(Fc)中分离DNA。使用琼脂糖凝胶电泳、溴化乙锭(EtBr)结合和熔解温度技术研究DNA损伤。

结果

与相应对照相比,经Al-M处理的老年新西兰兔的H和M显示出更高的DNA损伤,而Fc与相应对照相比显示出轻度DNA损伤。

结论

本研究切实提供了对该疾病在分子水平上的实质性理解,进而为简化潜在治疗策略提供了一个适当的平台。

关键词

阿尔茨海默病;苹果酸铝;动物模型;DNA损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd50/3299183/41a7ea1eaa74/jocmr-01-212-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd50/3299183/d765758e7689/jocmr-01-212-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd50/3299183/845c0ba5ab85/jocmr-01-212-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd50/3299183/57940a8f8796/jocmr-01-212-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd50/3299183/bd43588975e6/jocmr-01-212-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd50/3299183/40ac9e67016c/jocmr-01-212-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd50/3299183/de8631314544/jocmr-01-212-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd50/3299183/7cbf747ebfcb/jocmr-01-212-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd50/3299183/f5cf07b94327/jocmr-01-212-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd50/3299183/41a7ea1eaa74/jocmr-01-212-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd50/3299183/d765758e7689/jocmr-01-212-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd50/3299183/845c0ba5ab85/jocmr-01-212-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd50/3299183/57940a8f8796/jocmr-01-212-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd50/3299183/bd43588975e6/jocmr-01-212-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd50/3299183/40ac9e67016c/jocmr-01-212-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd50/3299183/de8631314544/jocmr-01-212-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd50/3299183/7cbf747ebfcb/jocmr-01-212-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd50/3299183/f5cf07b94327/jocmr-01-212-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bd50/3299183/41a7ea1eaa74/jocmr-01-212-g009.jpg

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