Mathematical model on Alzheimer's disease. Issue 1 (December 2016)

• Record Type: Journal Article
• Authors: Hao, Wenrui; Friedman, Avner
• Is Part Of: BMC systems biology. Volume 10:Issue 1(2016)
• Page Start: 1
• Page End: 18
• Publication Date: 2016-12
• Subjects: Alzheimer disease -- Mathematical modeling -- Drug treatment; Biological systems -- Periodicals; Biology -- Research -- Periodicals; Cell physiology -- Periodicals; Genes -- Analysis -- Periodicals; 571
• DOI: 10.1186/s12918-016-0348-2
• Languages: English
• ISSNs: 1752-0509

Abstract

Abstract 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 amyloidβ -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 amyloidβ 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-α inhibitor and anti amyloidβ could yield significant efficacy in slowing the progression of AD.