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Mathematical model on Alzheimer’s disease
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 β-peptides and intracellular neurofibrillary tangles o...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5116206/ https://www.ncbi.nlm.nih.gov/pubmed/27863488 http://dx.doi.org/10.1186/s12918-016-0348-2 |
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author | Hao, Wenrui Friedman, Avner |
author_facet | Hao, Wenrui Friedman, Avner |
author_sort | Hao, Wenrui |
collection | PubMed |
description | 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 β-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 β 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 amyloid β could yield significant efficacy in slowing the progression of AD. |
format | Online Article Text |
id | pubmed-5116206 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-51162062016-11-25 Mathematical model on Alzheimer’s disease Hao, Wenrui Friedman, Avner BMC Syst Biol Research Article 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 β-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 β 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 amyloid β could yield significant efficacy in slowing the progression of AD. BioMed Central 2016-11-18 /pmc/articles/PMC5116206/ /pubmed/27863488 http://dx.doi.org/10.1186/s12918-016-0348-2 Text en © The Author(s) 2016 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Article Hao, Wenrui Friedman, Avner Mathematical model on Alzheimer’s disease |
title | Mathematical model on Alzheimer’s disease |
title_full | Mathematical model on Alzheimer’s disease |
title_fullStr | Mathematical model on Alzheimer’s disease |
title_full_unstemmed | Mathematical model on Alzheimer’s disease |
title_short | Mathematical model on Alzheimer’s disease |
title_sort | mathematical model on alzheimer’s disease |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5116206/ https://www.ncbi.nlm.nih.gov/pubmed/27863488 http://dx.doi.org/10.1186/s12918-016-0348-2 |
work_keys_str_mv | AT haowenrui mathematicalmodelonalzheimersdisease AT friedmanavner mathematicalmodelonalzheimersdisease |