Traumatic brain injury in the presence of Aβ pathology affects neuronal survival, glial activation and autophagy

Abstract Traumatic brain injury (TBI) presents a widespread health problem in the elderly population. In addition to the acute injury, epidemiological studies have observed an increased probability and earlier onset of dementias in the elderly following TBI. However, the underlying mechanisms of the...

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Autores principales:	Linn Streubel-Gallasch, Marlena Zyśk, Chiara Beretta, Anna Erlandsson
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/7852d151364c4a9a8ae497162b6a2cc3
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spelling	oai:doaj.org-article:7852d151364c4a9a8ae497162b6a2cc32021-11-28T12:20:59ZTraumatic brain injury in the presence of Aβ pathology affects neuronal survival, glial activation and autophagy10.1038/s41598-021-02371-32045-2322https://doaj.org/article/7852d151364c4a9a8ae497162b6a2cc32021-11-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-02371-3https://doaj.org/toc/2045-2322Abstract Traumatic brain injury (TBI) presents a widespread health problem in the elderly population. In addition to the acute injury, epidemiological studies have observed an increased probability and earlier onset of dementias in the elderly following TBI. However, the underlying mechanisms of the connection between TBI and Alzheimer’s disease in the aged brain and potential exacerbating factors is still evolving. The aim of this study was to investigate cellular injury-induced processes in the presence of amyloid β (Aβ) pathology. For this purpose, a co-culture system of cortical stem-cell derived astrocytes, neurons and oligodendrocytes were exposed to Aβ42 protofibrils prior to a mechanically induced scratch injury. Cellular responses, including neurodegeneration, glial activation and autophagy was assessed by immunoblotting, immunocytochemistry, ELISA and transmission electron microscopy. Our results demonstrate that the combined burden of Aβ exposure and experimental TBI causes a decline in the number of neurons, the differential expression of the key astrocytic markers glial fibrillary acidic protein and S100 calcium-binding protein beta, mitochondrial alterations and prevents the upregulation of autophagy. Our study provides valuable information about the impact of TBI sustained in the presence of Aβ deposits and helps to advance the understanding of geriatric TBI on the cellular level.Linn Streubel-GallaschMarlena ZyśkChiara BerettaAnna ErlandssonNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-19 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Linn Streubel-Gallasch Marlena Zyśk Chiara Beretta Anna Erlandsson Traumatic brain injury in the presence of Aβ pathology affects neuronal survival, glial activation and autophagy
description	Abstract Traumatic brain injury (TBI) presents a widespread health problem in the elderly population. In addition to the acute injury, epidemiological studies have observed an increased probability and earlier onset of dementias in the elderly following TBI. However, the underlying mechanisms of the connection between TBI and Alzheimer’s disease in the aged brain and potential exacerbating factors is still evolving. The aim of this study was to investigate cellular injury-induced processes in the presence of amyloid β (Aβ) pathology. For this purpose, a co-culture system of cortical stem-cell derived astrocytes, neurons and oligodendrocytes were exposed to Aβ42 protofibrils prior to a mechanically induced scratch injury. Cellular responses, including neurodegeneration, glial activation and autophagy was assessed by immunoblotting, immunocytochemistry, ELISA and transmission electron microscopy. Our results demonstrate that the combined burden of Aβ exposure and experimental TBI causes a decline in the number of neurons, the differential expression of the key astrocytic markers glial fibrillary acidic protein and S100 calcium-binding protein beta, mitochondrial alterations and prevents the upregulation of autophagy. Our study provides valuable information about the impact of TBI sustained in the presence of Aβ deposits and helps to advance the understanding of geriatric TBI on the cellular level.
format	article
author	Linn Streubel-Gallasch Marlena Zyśk Chiara Beretta Anna Erlandsson
author_facet	Linn Streubel-Gallasch Marlena Zyśk Chiara Beretta Anna Erlandsson
author_sort	Linn Streubel-Gallasch
title	Traumatic brain injury in the presence of Aβ pathology affects neuronal survival, glial activation and autophagy
title_short	Traumatic brain injury in the presence of Aβ pathology affects neuronal survival, glial activation and autophagy
title_full	Traumatic brain injury in the presence of Aβ pathology affects neuronal survival, glial activation and autophagy
title_fullStr	Traumatic brain injury in the presence of Aβ pathology affects neuronal survival, glial activation and autophagy
title_full_unstemmed	Traumatic brain injury in the presence of Aβ pathology affects neuronal survival, glial activation and autophagy
title_sort	traumatic brain injury in the presence of aβ pathology affects neuronal survival, glial activation and autophagy
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/7852d151364c4a9a8ae497162b6a2cc3
work_keys_str_mv	AT linnstreubelgallasch traumaticbraininjuryinthepresenceofabpathologyaffectsneuronalsurvivalglialactivationandautophagy AT marlenazysk traumaticbraininjuryinthepresenceofabpathologyaffectsneuronalsurvivalglialactivationandautophagy AT chiaraberetta traumaticbraininjuryinthepresenceofabpathologyaffectsneuronalsurvivalglialactivationandautophagy AT annaerlandsson traumaticbraininjuryinthepresenceofabpathologyaffectsneuronalsurvivalglialactivationandautophagy
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Traumatic brain injury in the presence of Aβ pathology affects neuronal survival, glial activation and autophagy

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