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Platelets transport β-amyloid from the peripheral blood into the brain by destroying the blood-brain barrier to accelerate the process of Alzheimer's disease in mouse models
Extracellular aggregation of the β-amyloid (Aβ) peptide into toxic multimers in the brain is a prominent event occurring in the pathogenesis of Alzheimer’s disease (AD), and a large amount of Aβ in the blood is derived from platelets. Thus, we speculated that platelets may play an important role in...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Impact Journals
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7993748/ https://www.ncbi.nlm.nih.gov/pubmed/33668038 http://dx.doi.org/10.18632/aging.202662 |
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author | Wu, Tong Chen, Lizhi Zhou, Lingqi Xu, Jie Guo, Kaihua |
author_facet | Wu, Tong Chen, Lizhi Zhou, Lingqi Xu, Jie Guo, Kaihua |
author_sort | Wu, Tong |
collection | PubMed |
description | Extracellular aggregation of the β-amyloid (Aβ) peptide into toxic multimers in the brain is a prominent event occurring in the pathogenesis of Alzheimer’s disease (AD), and a large amount of Aβ in the blood is derived from platelets. Thus, we speculated that platelets may play an important role in the process of AD. We first investigated the changes in platelet Aβ secretion with age. Then, we injected platelets from aged amyloid precursor protein APP/PS1 mice into young C57 mice and assessed their memory capacity along with their brain and peripheral blood Aβ expression levels. The Aβ content in mouse platelets increased with age. Exogenously aged APP/PS1 platelets changed the permeability of the blood-brain barrier in vitro, accelerating Aβ deposition in the brain and increasing the Aβ content in peripheral blood, leading to learning and memory deficits in the recipient mice. Subsequently, aspirin was administered to mice as an inhibitor of platelet activation, which effectively alleviated these toxic processes. Finally, we chose an in vitro blood-brain barrier model to explore the possible cytotoxicity of these platelets. |
format | Online Article Text |
id | pubmed-7993748 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Impact Journals |
record_format | MEDLINE/PubMed |
spelling | pubmed-79937482021-04-06 Platelets transport β-amyloid from the peripheral blood into the brain by destroying the blood-brain barrier to accelerate the process of Alzheimer's disease in mouse models Wu, Tong Chen, Lizhi Zhou, Lingqi Xu, Jie Guo, Kaihua Aging (Albany NY) Research Paper Extracellular aggregation of the β-amyloid (Aβ) peptide into toxic multimers in the brain is a prominent event occurring in the pathogenesis of Alzheimer’s disease (AD), and a large amount of Aβ in the blood is derived from platelets. Thus, we speculated that platelets may play an important role in the process of AD. We first investigated the changes in platelet Aβ secretion with age. Then, we injected platelets from aged amyloid precursor protein APP/PS1 mice into young C57 mice and assessed their memory capacity along with their brain and peripheral blood Aβ expression levels. The Aβ content in mouse platelets increased with age. Exogenously aged APP/PS1 platelets changed the permeability of the blood-brain barrier in vitro, accelerating Aβ deposition in the brain and increasing the Aβ content in peripheral blood, leading to learning and memory deficits in the recipient mice. Subsequently, aspirin was administered to mice as an inhibitor of platelet activation, which effectively alleviated these toxic processes. Finally, we chose an in vitro blood-brain barrier model to explore the possible cytotoxicity of these platelets. Impact Journals 2021-03-05 /pmc/articles/PMC7993748/ /pubmed/33668038 http://dx.doi.org/10.18632/aging.202662 Text en Copyright: © 2021 Wu et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/3.0/) (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Paper Wu, Tong Chen, Lizhi Zhou, Lingqi Xu, Jie Guo, Kaihua Platelets transport β-amyloid from the peripheral blood into the brain by destroying the blood-brain barrier to accelerate the process of Alzheimer's disease in mouse models |
title | Platelets transport β-amyloid from the peripheral blood into the brain by destroying the blood-brain barrier to accelerate the process of Alzheimer's disease in mouse models |
title_full | Platelets transport β-amyloid from the peripheral blood into the brain by destroying the blood-brain barrier to accelerate the process of Alzheimer's disease in mouse models |
title_fullStr | Platelets transport β-amyloid from the peripheral blood into the brain by destroying the blood-brain barrier to accelerate the process of Alzheimer's disease in mouse models |
title_full_unstemmed | Platelets transport β-amyloid from the peripheral blood into the brain by destroying the blood-brain barrier to accelerate the process of Alzheimer's disease in mouse models |
title_short | Platelets transport β-amyloid from the peripheral blood into the brain by destroying the blood-brain barrier to accelerate the process of Alzheimer's disease in mouse models |
title_sort | platelets transport β-amyloid from the peripheral blood into the brain by destroying the blood-brain barrier to accelerate the process of alzheimer's disease in mouse models |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7993748/ https://www.ncbi.nlm.nih.gov/pubmed/33668038 http://dx.doi.org/10.18632/aging.202662 |
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