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Knee osteoarthritis accelerates amyloid beta deposition and neurodegeneration in a mouse model of Alzheimer’s disease

Knee osteoarthritis (OA) is characterized by knee cartilage degeneration and secondary bone hyperplasia, resulting in pain, stiffness, and gait disturbance. The relationship between knee OA and neurodegenerative diseases is still unclear. This study used an Alzheimer’s disease (AD) mouse model to ob...

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Autores principales: Gupta, Deepak Prasad, Lee, Young-Sun, Choe, Youngshik, Kim, Kun-Tae, Song, Gyun Jee, Hwang, Sun-Chul
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9809050/
https://www.ncbi.nlm.nih.gov/pubmed/36593507
http://dx.doi.org/10.1186/s13041-022-00986-9
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author Gupta, Deepak Prasad
Lee, Young-Sun
Choe, Youngshik
Kim, Kun-Tae
Song, Gyun Jee
Hwang, Sun-Chul
author_facet Gupta, Deepak Prasad
Lee, Young-Sun
Choe, Youngshik
Kim, Kun-Tae
Song, Gyun Jee
Hwang, Sun-Chul
author_sort Gupta, Deepak Prasad
collection PubMed
description Knee osteoarthritis (OA) is characterized by knee cartilage degeneration and secondary bone hyperplasia, resulting in pain, stiffness, and gait disturbance. The relationship between knee OA and neurodegenerative diseases is still unclear. This study used an Alzheimer’s disease (AD) mouse model to observe whether osteoarthritis accelerates dementia progression by analyzing brain histology and neuroinflammation. Knee OA was induced by destabilizing the medial meniscus (DMM) in control (WT) and AD (5xFAD) mice before pathological symptoms. Mouse knee joints were scanned with a micro-CT scanner. A sham operation was used as control. Motor and cognitive abilities were tested after OA induction. Neurodegeneration, β-amyloid plaque formation, and neuroinflammation were analyzed by immunostaining, Western blotting, and RT-PCR in brain tissues. Compared with sham controls, OA in AD mice increased inflammatory cytokine levels in brain tissues. Furthermore, OA significantly increased β-amyloid deposition and neuronal loss in AD mice compared to sham controls. In conclusion, knee OA accelerated amyloid plaque deposition and neurodegeneration in AD-OA mice, suggesting that OA is a risk factor for AD.
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spelling pubmed-98090502023-01-04 Knee osteoarthritis accelerates amyloid beta deposition and neurodegeneration in a mouse model of Alzheimer’s disease Gupta, Deepak Prasad Lee, Young-Sun Choe, Youngshik Kim, Kun-Tae Song, Gyun Jee Hwang, Sun-Chul Mol Brain Research Knee osteoarthritis (OA) is characterized by knee cartilage degeneration and secondary bone hyperplasia, resulting in pain, stiffness, and gait disturbance. The relationship between knee OA and neurodegenerative diseases is still unclear. This study used an Alzheimer’s disease (AD) mouse model to observe whether osteoarthritis accelerates dementia progression by analyzing brain histology and neuroinflammation. Knee OA was induced by destabilizing the medial meniscus (DMM) in control (WT) and AD (5xFAD) mice before pathological symptoms. Mouse knee joints were scanned with a micro-CT scanner. A sham operation was used as control. Motor and cognitive abilities were tested after OA induction. Neurodegeneration, β-amyloid plaque formation, and neuroinflammation were analyzed by immunostaining, Western blotting, and RT-PCR in brain tissues. Compared with sham controls, OA in AD mice increased inflammatory cytokine levels in brain tissues. Furthermore, OA significantly increased β-amyloid deposition and neuronal loss in AD mice compared to sham controls. In conclusion, knee OA accelerated amyloid plaque deposition and neurodegeneration in AD-OA mice, suggesting that OA is a risk factor for AD. BioMed Central 2023-01-02 /pmc/articles/PMC9809050/ /pubmed/36593507 http://dx.doi.org/10.1186/s13041-022-00986-9 Text en © The Author(s) 2023 https://creativecommons.org/licenses/by/4.0/Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
spellingShingle Research
Gupta, Deepak Prasad
Lee, Young-Sun
Choe, Youngshik
Kim, Kun-Tae
Song, Gyun Jee
Hwang, Sun-Chul
Knee osteoarthritis accelerates amyloid beta deposition and neurodegeneration in a mouse model of Alzheimer’s disease
title Knee osteoarthritis accelerates amyloid beta deposition and neurodegeneration in a mouse model of Alzheimer’s disease
title_full Knee osteoarthritis accelerates amyloid beta deposition and neurodegeneration in a mouse model of Alzheimer’s disease
title_fullStr Knee osteoarthritis accelerates amyloid beta deposition and neurodegeneration in a mouse model of Alzheimer’s disease
title_full_unstemmed Knee osteoarthritis accelerates amyloid beta deposition and neurodegeneration in a mouse model of Alzheimer’s disease
title_short Knee osteoarthritis accelerates amyloid beta deposition and neurodegeneration in a mouse model of Alzheimer’s disease
title_sort knee osteoarthritis accelerates amyloid beta deposition and neurodegeneration in a mouse model of alzheimer’s disease
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9809050/
https://www.ncbi.nlm.nih.gov/pubmed/36593507
http://dx.doi.org/10.1186/s13041-022-00986-9
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