Mathematical model on Alzheimer's disease

被引:94
|
作者
Hao, Wenrui [1 ]
Friedman, Avner [2 ,3 ]
机构
[1] Penn State Univ, Dept Math, University Pk, PA 16802 USA
[2] Ohio State Univ, Math Biosci Inst, Columbus, OH 43210 USA
[3] Ohio State Univ, Dept Math, Columbus, OH 43210 USA
基金
美国国家科学基金会;
关键词
Alzheimer disease; Mathematical modeling; Drug treatment; AMYLOID-BETA PEPTIDES; TUMOR-NECROSIS-FACTOR; A-BETA; CHROMATIN PROTEIN; CCL2; SYNTHESIS; TAU PATHOLOGY; MICROGLIA; CELLS; BRAIN; MACROPHAGES;
D O I
10.1186/s12918-016-0348-2
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
Background: Alzheimer disease (AD) is a progressive neurodegenerative disease that destroys memory and cognitive skills. AD is characterized by the presence of two types of neuropathological hallmarks: extracellular plaques consisting of amyloid beta-peptides and intracellular neurofibrillary tangles of hyperphosphorylated tau proteins. The disease affects 5 million people in the United States and 44 million world-wide. Currently there is no drug that can cure, stop or even slow the progression of the disease. If no cure is found, by 2050 the number of alzheimer's patients in the U.S. will reach 15 million and the cost of caring for them will exceed $ 1 trillion annually. Results: The present paper develops a mathematical model of AD that includes neurons, astrocytes, microglias and peripheral macrophages, as well as amyloid beta aggregation and hyperphosphorylated tau proteins. The model is represented by a system of partial differential equations. The model is used to simulate the effect of drugs that either failed in clinical trials, or are currently in clinical trials. Conclusions: Based on these simulations it is suggested that combined therapy with TNF-alpha inhibitor and anti amyloid beta could yield significant efficacy in slowing the progression of AD.
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收藏
页数:18
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