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Rosmarinic acid suppresses Alzheimer’s disease development by reducing amyloid β aggregation by increasing monoamine secretion
A new mechanism is revealed by which a polyphenol, rosmarinic acid (RA), suppresses amyloid β (Aβ) accumulation in mice. Here we examined the brains of mice (Alzheimer’s disease model) using DNA microarray analysis and revealed that the dopamine (DA)-signaling pathway was enhanced in the group fed R...
Autores principales: | , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6581955/ https://www.ncbi.nlm.nih.gov/pubmed/31213631 http://dx.doi.org/10.1038/s41598-019-45168-1 |
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author | Hase, Tomoki Shishido, Syun Yamamoto, So Yamashita, Rei Nukima, Haruka Taira, Shu Toyoda, Tsudoi Abe, Keiko Hamaguchi, Tsuyoshi Ono, Kenjiro Noguchi-Shinohara, Moeko Yamada, Masahito Kobayashi, Shoko |
author_facet | Hase, Tomoki Shishido, Syun Yamamoto, So Yamashita, Rei Nukima, Haruka Taira, Shu Toyoda, Tsudoi Abe, Keiko Hamaguchi, Tsuyoshi Ono, Kenjiro Noguchi-Shinohara, Moeko Yamada, Masahito Kobayashi, Shoko |
author_sort | Hase, Tomoki |
collection | PubMed |
description | A new mechanism is revealed by which a polyphenol, rosmarinic acid (RA), suppresses amyloid β (Aβ) accumulation in mice. Here we examined the brains of mice (Alzheimer’s disease model) using DNA microarray analysis and revealed that the dopamine (DA)-signaling pathway was enhanced in the group fed RA versus controls. In the cerebral cortex, the levels of monoamines, such as norepinephrine, 3,4-dihydroxyphenylacetic acid, DA, and levodopa, increased after RA feeding. The expression of DA-degrading enzymes, such as monoamine oxidase B (Maob), was significantly downregulated in the substantia nigra and ventral tegmental area, both DA synthesis regions. Following in vitro studies showing that monoamines inhibited Aβ aggregation, this in vivo study, in which RA intake increased concentration of monoamine by reducing Maob gene expression, builds on that knowledge by demonstrating that monoamines suppress Aβ aggregation. In conclusion, RA-initiated monoamine increase in the brain may beneficially act against AD. |
format | Online Article Text |
id | pubmed-6581955 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-65819552019-06-26 Rosmarinic acid suppresses Alzheimer’s disease development by reducing amyloid β aggregation by increasing monoamine secretion Hase, Tomoki Shishido, Syun Yamamoto, So Yamashita, Rei Nukima, Haruka Taira, Shu Toyoda, Tsudoi Abe, Keiko Hamaguchi, Tsuyoshi Ono, Kenjiro Noguchi-Shinohara, Moeko Yamada, Masahito Kobayashi, Shoko Sci Rep Article A new mechanism is revealed by which a polyphenol, rosmarinic acid (RA), suppresses amyloid β (Aβ) accumulation in mice. Here we examined the brains of mice (Alzheimer’s disease model) using DNA microarray analysis and revealed that the dopamine (DA)-signaling pathway was enhanced in the group fed RA versus controls. In the cerebral cortex, the levels of monoamines, such as norepinephrine, 3,4-dihydroxyphenylacetic acid, DA, and levodopa, increased after RA feeding. The expression of DA-degrading enzymes, such as monoamine oxidase B (Maob), was significantly downregulated in the substantia nigra and ventral tegmental area, both DA synthesis regions. Following in vitro studies showing that monoamines inhibited Aβ aggregation, this in vivo study, in which RA intake increased concentration of monoamine by reducing Maob gene expression, builds on that knowledge by demonstrating that monoamines suppress Aβ aggregation. In conclusion, RA-initiated monoamine increase in the brain may beneficially act against AD. Nature Publishing Group UK 2019-06-18 /pmc/articles/PMC6581955/ /pubmed/31213631 http://dx.doi.org/10.1038/s41598-019-45168-1 Text en © The Author(s) 2019 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as 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 images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Hase, Tomoki Shishido, Syun Yamamoto, So Yamashita, Rei Nukima, Haruka Taira, Shu Toyoda, Tsudoi Abe, Keiko Hamaguchi, Tsuyoshi Ono, Kenjiro Noguchi-Shinohara, Moeko Yamada, Masahito Kobayashi, Shoko Rosmarinic acid suppresses Alzheimer’s disease development by reducing amyloid β aggregation by increasing monoamine secretion |
title | Rosmarinic acid suppresses Alzheimer’s disease development by reducing amyloid β aggregation by increasing monoamine secretion |
title_full | Rosmarinic acid suppresses Alzheimer’s disease development by reducing amyloid β aggregation by increasing monoamine secretion |
title_fullStr | Rosmarinic acid suppresses Alzheimer’s disease development by reducing amyloid β aggregation by increasing monoamine secretion |
title_full_unstemmed | Rosmarinic acid suppresses Alzheimer’s disease development by reducing amyloid β aggregation by increasing monoamine secretion |
title_short | Rosmarinic acid suppresses Alzheimer’s disease development by reducing amyloid β aggregation by increasing monoamine secretion |
title_sort | rosmarinic acid suppresses alzheimer’s disease development by reducing amyloid β aggregation by increasing monoamine secretion |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6581955/ https://www.ncbi.nlm.nih.gov/pubmed/31213631 http://dx.doi.org/10.1038/s41598-019-45168-1 |
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