Peak ependymal cell stretch overlaps with the onset locations of periventricular white matter lesions

Abstract Deep and periventricular white matter hyperintensities (dWMH/pvWMH) are bright appearing white matter tissue lesions in T2-weighted fluid attenuated inversion recovery magnetic resonance images and are frequent observations in the aging human brain. While early stages of these white matter...

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Autores principales:	Valery L. Visser, Henry Rusinek, Johannes Weickenmeier
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/7f3b023c45314104970af1d8861fdff1
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spelling	oai:doaj.org-article:7f3b023c45314104970af1d8861fdff12021-11-14T12:23:18ZPeak ependymal cell stretch overlaps with the onset locations of periventricular white matter lesions10.1038/s41598-021-00610-12045-2322https://doaj.org/article/7f3b023c45314104970af1d8861fdff12021-11-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-00610-1https://doaj.org/toc/2045-2322Abstract Deep and periventricular white matter hyperintensities (dWMH/pvWMH) are bright appearing white matter tissue lesions in T2-weighted fluid attenuated inversion recovery magnetic resonance images and are frequent observations in the aging human brain. While early stages of these white matter lesions are only weakly associated with cognitive impairment, their progressive growth is a strong indicator for long-term functional decline. DWMHs are typically associated with vascular degeneration in diffuse white matter locations; for pvWMHs, however, no unifying theory exists to explain their consistent onset around the horns of the lateral ventricles. We use patient imaging data to create anatomically accurate finite element models of the lateral ventricles, white and gray matter, and cerebrospinal fluid, as well as to reconstruct their WMH volumes. We simulated the mechanical loading of the ependymal cells forming the primary brain-fluid interface, the ventricular wall, and its surrounding tissues at peak ventricular pressure during the hemodynamic cycle. We observe that both the maximum principal tissue strain and the largest ependymal cell stretch consistently localize in the anterior and posterior horns. Our simulations show that ependymal cells experience a loading state that causes the ventricular wall to be stretched thin. Moreover, we show that maximum wall loading coincides with the pvWMH locations observed in our patient scans. These results warrant further analysis of white matter pathology in the periventricular zone that includes a mechanics-driven deterioration model for the ventricular wall.Valery L. VisserHenry RusinekJohannes WeickenmeierNature 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 Valery L. Visser Henry Rusinek Johannes Weickenmeier Peak ependymal cell stretch overlaps with the onset locations of periventricular white matter lesions
description	Abstract Deep and periventricular white matter hyperintensities (dWMH/pvWMH) are bright appearing white matter tissue lesions in T2-weighted fluid attenuated inversion recovery magnetic resonance images and are frequent observations in the aging human brain. While early stages of these white matter lesions are only weakly associated with cognitive impairment, their progressive growth is a strong indicator for long-term functional decline. DWMHs are typically associated with vascular degeneration in diffuse white matter locations; for pvWMHs, however, no unifying theory exists to explain their consistent onset around the horns of the lateral ventricles. We use patient imaging data to create anatomically accurate finite element models of the lateral ventricles, white and gray matter, and cerebrospinal fluid, as well as to reconstruct their WMH volumes. We simulated the mechanical loading of the ependymal cells forming the primary brain-fluid interface, the ventricular wall, and its surrounding tissues at peak ventricular pressure during the hemodynamic cycle. We observe that both the maximum principal tissue strain and the largest ependymal cell stretch consistently localize in the anterior and posterior horns. Our simulations show that ependymal cells experience a loading state that causes the ventricular wall to be stretched thin. Moreover, we show that maximum wall loading coincides with the pvWMH locations observed in our patient scans. These results warrant further analysis of white matter pathology in the periventricular zone that includes a mechanics-driven deterioration model for the ventricular wall.
format	article
author	Valery L. Visser Henry Rusinek Johannes Weickenmeier
author_facet	Valery L. Visser Henry Rusinek Johannes Weickenmeier
author_sort	Valery L. Visser
title	Peak ependymal cell stretch overlaps with the onset locations of periventricular white matter lesions
title_short	Peak ependymal cell stretch overlaps with the onset locations of periventricular white matter lesions
title_full	Peak ependymal cell stretch overlaps with the onset locations of periventricular white matter lesions
title_fullStr	Peak ependymal cell stretch overlaps with the onset locations of periventricular white matter lesions
title_full_unstemmed	Peak ependymal cell stretch overlaps with the onset locations of periventricular white matter lesions
title_sort	peak ependymal cell stretch overlaps with the onset locations of periventricular white matter lesions
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/7f3b023c45314104970af1d8861fdff1
work_keys_str_mv	AT valerylvisser peakependymalcellstretchoverlapswiththeonsetlocationsofperiventricularwhitematterlesions AT henryrusinek peakependymalcellstretchoverlapswiththeonsetlocationsofperiventricularwhitematterlesions AT johannesweickenmeier peakependymalcellstretchoverlapswiththeonsetlocationsofperiventricularwhitematterlesions
_version_	1718429237900214272

Peak ependymal cell stretch overlaps with the onset locations of periventricular white matter lesions

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