期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 24, 期 8, 页码 -出版社
MDPI
DOI: 10.3390/ijms24087258
关键词
Alzheimer's disease; amyloid beta-protein; tau proteins; heme; heme oxygenase
Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by neurofibrillary tangles, amyloid beta plaque deposition, and neurodegeneration. Genetic mutations, inflammation, blood-brain barrier impairment, mitochondrial dysfunction, oxidative stress, and metal ion imbalance are associated with AD progression. Recent studies have shown a link between altered heme metabolism and AD. Understanding the underlying mechanisms and identifying therapeutic targets is crucial for AD drug development. This review discusses common alterations in AD, potential therapeutic targets, mathematical models, and treatment strategies.
Alzheimer's disease (AD) is a progressive neurodegenerative disorder that leads to dementia and patient death. AD is characterized by intracellular neurofibrillary tangles, extracellular amyloid beta (A beta) plaque deposition, and neurodegeneration. Diverse alterations have been associated with AD progression, including genetic mutations, neuroinflammation, blood-brain barrier (BBB) impairment, mitochondrial dysfunction, oxidative stress, and metal ion imbalance.Additionally, recent studies have shown an association between altered heme metabolism and AD. Unfortunately, decades of research and drug development have not produced any effective treatments for AD. Therefore, understanding the cellular and molecular mechanisms underlying AD pathology and identifying potential therapeutic targets are crucial for AD drug development. This review discusses the most common alterations associated with AD and promising therapeutic targets for AD drug discovery. Furthermore, it highlights the role of heme in AD development and summarizes mathematical models of AD, including a stochastic mathematical model of AD and mathematical models of the effect of A beta on AD. We also summarize the potential treatment strategies that these models can offer in clinical trials.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据