N-Acetyl-l-leucine improves functional recovery and attenuates cortical cell death and neuroinflammation after traumatic brain injury in mice

Abstract Traumatic brain injury (TBI) is a major cause of mortality and long-term disability around the world. Even mild to moderate TBI can lead to lifelong neurological impairment due to acute and progressive neurodegeneration and neuroinflammation induced by the injury. Thus, the discovery of nov...

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Autores principales:	Nivedita Hegdekar, Marta M. Lipinski, Chinmoy Sarkar
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/2ccb4c4b9e234e9994a993a0c6f1c956
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spelling	oai:doaj.org-article:2ccb4c4b9e234e9994a993a0c6f1c9562021-12-02T16:55:24ZN-Acetyl-l-leucine improves functional recovery and attenuates cortical cell death and neuroinflammation after traumatic brain injury in mice10.1038/s41598-021-88693-82045-2322https://doaj.org/article/2ccb4c4b9e234e9994a993a0c6f1c9562021-04-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-88693-8https://doaj.org/toc/2045-2322Abstract Traumatic brain injury (TBI) is a major cause of mortality and long-term disability around the world. Even mild to moderate TBI can lead to lifelong neurological impairment due to acute and progressive neurodegeneration and neuroinflammation induced by the injury. Thus, the discovery of novel treatments which can be used as early therapeutic interventions following TBI is essential to restrict neuronal cell death and neuroinflammation. We demonstrate that orally administered N-acetyl-l-leucine (NALL) significantly improved motor and cognitive outcomes in the injured mice, led to the attenuation of cell death, and reduced the expression of neuroinflammatory markers after controlled cortical impact (CCI) induced experimental TBI in mice. Our data indicate that partial restoration of autophagy flux mediated by NALL may account for the positive effect of treatment in the injured mouse brain. Taken together, our study indicates that treatment with NALL would be expected to improve neurological function after injury by restricting cortical cell death and neuroinflammation. Therefore, NALL is a promising novel, neuroprotective drug candidate for the treatment of TBI.Nivedita HegdekarMarta M. LipinskiChinmoy SarkarNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-13 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Nivedita Hegdekar Marta M. Lipinski Chinmoy Sarkar N-Acetyl-l-leucine improves functional recovery and attenuates cortical cell death and neuroinflammation after traumatic brain injury in mice
description	Abstract Traumatic brain injury (TBI) is a major cause of mortality and long-term disability around the world. Even mild to moderate TBI can lead to lifelong neurological impairment due to acute and progressive neurodegeneration and neuroinflammation induced by the injury. Thus, the discovery of novel treatments which can be used as early therapeutic interventions following TBI is essential to restrict neuronal cell death and neuroinflammation. We demonstrate that orally administered N-acetyl-l-leucine (NALL) significantly improved motor and cognitive outcomes in the injured mice, led to the attenuation of cell death, and reduced the expression of neuroinflammatory markers after controlled cortical impact (CCI) induced experimental TBI in mice. Our data indicate that partial restoration of autophagy flux mediated by NALL may account for the positive effect of treatment in the injured mouse brain. Taken together, our study indicates that treatment with NALL would be expected to improve neurological function after injury by restricting cortical cell death and neuroinflammation. Therefore, NALL is a promising novel, neuroprotective drug candidate for the treatment of TBI.
format	article
author	Nivedita Hegdekar Marta M. Lipinski Chinmoy Sarkar
author_facet	Nivedita Hegdekar Marta M. Lipinski Chinmoy Sarkar
author_sort	Nivedita Hegdekar
title	N-Acetyl-l-leucine improves functional recovery and attenuates cortical cell death and neuroinflammation after traumatic brain injury in mice
title_short	N-Acetyl-l-leucine improves functional recovery and attenuates cortical cell death and neuroinflammation after traumatic brain injury in mice
title_full	N-Acetyl-l-leucine improves functional recovery and attenuates cortical cell death and neuroinflammation after traumatic brain injury in mice
title_fullStr	N-Acetyl-l-leucine improves functional recovery and attenuates cortical cell death and neuroinflammation after traumatic brain injury in mice
title_full_unstemmed	N-Acetyl-l-leucine improves functional recovery and attenuates cortical cell death and neuroinflammation after traumatic brain injury in mice
title_sort	n-acetyl-l-leucine improves functional recovery and attenuates cortical cell death and neuroinflammation after traumatic brain injury in mice
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/2ccb4c4b9e234e9994a993a0c6f1c956
work_keys_str_mv	AT niveditahegdekar nacetyllleucineimprovesfunctionalrecoveryandattenuatescorticalcelldeathandneuroinflammationaftertraumaticbraininjuryinmice AT martamlipinski nacetyllleucineimprovesfunctionalrecoveryandattenuatescorticalcelldeathandneuroinflammationaftertraumaticbraininjuryinmice AT chinmoysarkar nacetyllleucineimprovesfunctionalrecoveryandattenuatescorticalcelldeathandneuroinflammationaftertraumaticbraininjuryinmice
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N-Acetyl-l-leucine improves functional recovery and attenuates cortical cell death and neuroinflammation after traumatic brain injury in mice

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