表观遗传学
神经毒性
组蛋白
DNA甲基化
疾病
生物
小RNA
非编码RNA
遗传倾向
机制(生物学)
遗传学
神经科学
生物信息学
基因
计算生物学
医学
毒性
基因表达
病理
内科学
哲学
认识论
标识
DOI:10.1007/978-981-13-1370-7_10
摘要
This chapter primarily focuses on two key aspects related to aluminum neurotoxicity and its mechanism in Alzheimer's disease (AD), which are genetic susceptibility and epigenetic modification. The toxicity of aluminum has been confirmed from plant experiments, animal experiments, in vitro experiments, and epidemiological studies. However, the mechanisms underlying this phenomenon have largely remained elusive. Furthermore, there are more and more genetic factors that have been found to be strongly implicated for causing or increasing the risk of AD development and have been proved to be associated with the neurotoxicity of Al and play a significant role in the initiation and progression of AD. Epigenetics provide a bridge between genes and environment to improve our understanding on the etiology of AD. Al can modify the epigenetic status by DNA methylation, histone modifications, and noncoding RNAs and might thereby contribute to the pathophysiology of AD. However, very little is known about exact epigenetic patterns in AD.
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