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Aging and Alzheimer’s disease: Comparison and associations from molecular to system level
Alzheimer's disease is the most prevalent cause of dementia, which is defined by the combined presence of amyloid and tau, but researchers are gradually moving away from the simple assumption of linear causality proposed by the original amyloid hypothesis. Aging is the main risk factor for Alzh...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6156542/ https://www.ncbi.nlm.nih.gov/pubmed/29963744 http://dx.doi.org/10.1111/acel.12802 |
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author | Xia, Xian Jiang, Quanlong McDermott, Joseph Han, Jing‐Dong J. |
author_facet | Xia, Xian Jiang, Quanlong McDermott, Joseph Han, Jing‐Dong J. |
author_sort | Xia, Xian |
collection | PubMed |
description | Alzheimer's disease is the most prevalent cause of dementia, which is defined by the combined presence of amyloid and tau, but researchers are gradually moving away from the simple assumption of linear causality proposed by the original amyloid hypothesis. Aging is the main risk factor for Alzheimer's disease that cannot be explained by amyloid hypothesis. To evaluate how aging and Alzheimer's disease are intrinsically interwoven with each other, we review and summarize evidence from molecular, cellular, and system level. In particular, we focus on study designs, treatments, or interventions in Alzheimer's disease that could also be insightful in aging and vice versa. |
format | Online Article Text |
id | pubmed-6156542 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-61565422018-10-01 Aging and Alzheimer’s disease: Comparison and associations from molecular to system level Xia, Xian Jiang, Quanlong McDermott, Joseph Han, Jing‐Dong J. Aging Cell Reviews Alzheimer's disease is the most prevalent cause of dementia, which is defined by the combined presence of amyloid and tau, but researchers are gradually moving away from the simple assumption of linear causality proposed by the original amyloid hypothesis. Aging is the main risk factor for Alzheimer's disease that cannot be explained by amyloid hypothesis. To evaluate how aging and Alzheimer's disease are intrinsically interwoven with each other, we review and summarize evidence from molecular, cellular, and system level. In particular, we focus on study designs, treatments, or interventions in Alzheimer's disease that could also be insightful in aging and vice versa. John Wiley and Sons Inc. 2018-07-02 2018-10 /pmc/articles/PMC6156542/ /pubmed/29963744 http://dx.doi.org/10.1111/acel.12802 Text en © 2018 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Reviews Xia, Xian Jiang, Quanlong McDermott, Joseph Han, Jing‐Dong J. Aging and Alzheimer’s disease: Comparison and associations from molecular to system level |
title | Aging and Alzheimer’s disease: Comparison and associations from molecular to system level |
title_full | Aging and Alzheimer’s disease: Comparison and associations from molecular to system level |
title_fullStr | Aging and Alzheimer’s disease: Comparison and associations from molecular to system level |
title_full_unstemmed | Aging and Alzheimer’s disease: Comparison and associations from molecular to system level |
title_short | Aging and Alzheimer’s disease: Comparison and associations from molecular to system level |
title_sort | aging and alzheimer’s disease: comparison and associations from molecular to system level |
topic | Reviews |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6156542/ https://www.ncbi.nlm.nih.gov/pubmed/29963744 http://dx.doi.org/10.1111/acel.12802 |
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