Recent Development in the Understanding of Molecular and Cellular Mechanisms Underlying the Etiopathogenesis of Alzheimer's Disease

被引:17
|
作者
Afsar, Atefeh [1 ]
Castro, Maria del Carmen Chacon [1 ]
Soladogun, Adedamola Saidi [1 ]
Zhang, Li [1 ]
机构
[1] Univ Texas Dallas, Dept Biol Sci, Richardson, TX 75080 USA
关键词
Alzheimer's disease; amyloid beta-protein; tau proteins; heme; heme oxygenase; AMYLOID-BETA-PEPTIDE; BLOOD-BRAIN-BARRIER; ABNORMAL MITOCHONDRIAL DYNAMICS; MILD COGNITIVE IMPAIRMENT; GENOME-WIDE ASSOCIATION; TUMOR-NECROSIS-FACTOR; C-REACTIVE PROTEIN; CENTRAL CHOLINERGIC NEURONS; RADICAL OXIDATIVE STRESS; TRANSGENIC MOUSE MODEL;
D O I
10.3390/ijms24087258
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页数:49
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