Microglial morphology in Alzheimer’s disease and after Aβ immunotherapy

Abstract Microglia are the brain immune cells and their function is highly dependent on cell motility. It was hypothesised that morphological variability leads to differences in motility, ultimately impacting on the microglial function. Here, we assessed microglial morphology in 32 controls, 44 Alzh...

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Autores principales:	Diana K. Franco-Bocanegra, Yamina Gourari, Ciaran McAuley, David S. Chatelet, David A. Johnston, James A. R. Nicoll, Delphine Boche
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/f86008062e354063b1e13b8592a0398e
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spelling	oai:doaj.org-article:f86008062e354063b1e13b8592a0398e2021-12-02T18:49:36ZMicroglial morphology in Alzheimer’s disease and after Aβ immunotherapy10.1038/s41598-021-95535-02045-2322https://doaj.org/article/f86008062e354063b1e13b8592a0398e2021-08-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-95535-0https://doaj.org/toc/2045-2322Abstract Microglia are the brain immune cells and their function is highly dependent on cell motility. It was hypothesised that morphological variability leads to differences in motility, ultimately impacting on the microglial function. Here, we assessed microglial morphology in 32 controls, 44 Alzheimer’s disease (AD) cases and 16 AD cases from patients immunised against Aβ42 (iAD) using 2D and 3D approaches. Our 2D assessment showed an increased number of microglia in iAD vs. AD (P = 0.032) and controls (P = 0.018). Ramified microglia were fewer in AD vs. controls (P = 0.041) but increased in iAD compared to AD (P < 0.001) and controls (P = 0.006). 3D reconstructions highlighted larger cell bodies in AD vs. controls (P = 0.049) and increased total process length in iAD vs. AD (P = 0.032), with negative correlations detected for pan-Aβ load with total process length (P < 0.001) in AD and number of primary processes (P = 0.043) in iAD. In summary, reactive/amoeboid microglia are the most represented population in the aged human brain. AD does not affect the number of microglia, but the ramified population is decreased adopting a more reactive morphology. Aβ removal by immunotherapy leads to increased ramified microglia, implying that the cells retain plasticity in an aged disease brain meriting further investigation.Diana K. Franco-BocanegraYamina GourariCiaran McAuleyDavid S. ChateletDavid A. JohnstonJames A. R. NicollDelphine BocheNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-12 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Diana K. Franco-Bocanegra Yamina Gourari Ciaran McAuley David S. Chatelet David A. Johnston James A. R. Nicoll Delphine Boche Microglial morphology in Alzheimer’s disease and after Aβ immunotherapy
description	Abstract Microglia are the brain immune cells and their function is highly dependent on cell motility. It was hypothesised that morphological variability leads to differences in motility, ultimately impacting on the microglial function. Here, we assessed microglial morphology in 32 controls, 44 Alzheimer’s disease (AD) cases and 16 AD cases from patients immunised against Aβ42 (iAD) using 2D and 3D approaches. Our 2D assessment showed an increased number of microglia in iAD vs. AD (P = 0.032) and controls (P = 0.018). Ramified microglia were fewer in AD vs. controls (P = 0.041) but increased in iAD compared to AD (P < 0.001) and controls (P = 0.006). 3D reconstructions highlighted larger cell bodies in AD vs. controls (P = 0.049) and increased total process length in iAD vs. AD (P = 0.032), with negative correlations detected for pan-Aβ load with total process length (P < 0.001) in AD and number of primary processes (P = 0.043) in iAD. In summary, reactive/amoeboid microglia are the most represented population in the aged human brain. AD does not affect the number of microglia, but the ramified population is decreased adopting a more reactive morphology. Aβ removal by immunotherapy leads to increased ramified microglia, implying that the cells retain plasticity in an aged disease brain meriting further investigation.
format	article
author	Diana K. Franco-Bocanegra Yamina Gourari Ciaran McAuley David S. Chatelet David A. Johnston James A. R. Nicoll Delphine Boche
author_facet	Diana K. Franco-Bocanegra Yamina Gourari Ciaran McAuley David S. Chatelet David A. Johnston James A. R. Nicoll Delphine Boche
author_sort	Diana K. Franco-Bocanegra
title	Microglial morphology in Alzheimer’s disease and after Aβ immunotherapy
title_short	Microglial morphology in Alzheimer’s disease and after Aβ immunotherapy
title_full	Microglial morphology in Alzheimer’s disease and after Aβ immunotherapy
title_fullStr	Microglial morphology in Alzheimer’s disease and after Aβ immunotherapy
title_full_unstemmed	Microglial morphology in Alzheimer’s disease and after Aβ immunotherapy
title_sort	microglial morphology in alzheimer’s disease and after aβ immunotherapy
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/f86008062e354063b1e13b8592a0398e
work_keys_str_mv	AT dianakfrancobocanegra microglialmorphologyinalzheimersdiseaseandafterabimmunotherapy AT yaminagourari microglialmorphologyinalzheimersdiseaseandafterabimmunotherapy AT ciaranmcauley microglialmorphologyinalzheimersdiseaseandafterabimmunotherapy AT davidschatelet microglialmorphologyinalzheimersdiseaseandafterabimmunotherapy AT davidajohnston microglialmorphologyinalzheimersdiseaseandafterabimmunotherapy AT jamesarnicoll microglialmorphologyinalzheimersdiseaseandafterabimmunotherapy AT delphineboche microglialmorphologyinalzheimersdiseaseandafterabimmunotherapy
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Microglial morphology in Alzheimer’s disease and after Aβ immunotherapy

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