Abstract
Neuropathology and Applied NeurobiologyVolume 44, Issue 7 p. 747-748 ErratumFree Access Age-associated changes in the blood-brain barrier: comparative studies in human and mouse This article corrects the following: Age-associated changes in the blood-brain barrier: comparative studies in human and mouse E. F. Goodall, C. Wang, J. E. Simpson, D. J. Baker, D. R. Drew, P. R. Heath, M. J. Saffrey, I. A. Romero, S. B. Wharton, Volume 44Issue 3Neuropathology and Applied Neurobiology pages: 328-340 First Published online: May 29, 2017 First published: 20 November 2018 https://doi.org/10.1111/nan.12515AboutSectionsPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat Following the publication of the above article in Neuropathology and Applied Neurobiology 44: 328–340; April 1, we would like to correct the axis labels of Figures 4D,F and 5B,D. The axis labels should reflect ‘Age (years)’ instead of ‘Age (months)’. We have now changed the axis labels in the above mentioned figures and the correct figures are shown below. Figure 4Open in figure viewerPowerPoint Age-associated changes in glial pathology. (A) GFAP immunolabelling of astrocytes in the mouse brain. (B) GFAP area immunoreactivity correlates with age in all but the youngest age group of the mouse cohort (P = 0.016). (C) GFAP immunolabelling of astrocytes in the human brain. (D) In the ageing human cohort, semiquantitative assessment of gliosis in the cortex expression demonstrates an association with age (P = 0.003). (E) Iba-1+ microglia in the human brain. (F) In contrast to GFAP, no age-associated changes in Iba-1 expression were detected. Scale bar represents 50 lm in A,C,E. Figure 5Open in figure viewerPowerPoint Age-associated changes in vascular pathology. (A) CD31 immunolabelling of cerebral vessels in the human cortex. (B) No significant age-associated changes in microvascular density were detected. (C) PCGFRb+ pericytes (brown) are intimately associated with vessels (PAS, red). (D) There was no significant difference in the pericyte coverage of vessels in the youngest vs. the oldest group. Scale bar represents 50 lm. We apologize for this error. Reference 1Goodall EF, Wang C, Simpson JE, Baker DJ, Drew DR, Heath PR, et al. Age-associated changes in the blood-brain barrier: comparative studies in human and mouse. Neuropathol Appl Neurobiol 2018; 44: 328– 40 Volume44, Issue7December 2018Pages 747-748 FiguresReferencesRelatedInformation
Highlights
The mechanisms underlying central nervous system (CNS) dysfunction and cognitive deterioration during ageing are complex
Within the cortex and cerebellum quantification of the number of breaks in the blood– brain barrier (BBB) showed a significant difference between groups (KW: cortex P = 0.012, cerebellum P = 0.025), with a significant trend to increased number of breaks associated with age (JT: cortex P < 0.001, cerebellum P < 0.001) (Figure 2C,E)
Within the cortex and cerebellum quantification of BBB break length showed a significant difference between groups (KW: cortex P = 0.011, cerebellum P = 0.019), with a significant trend to increased break length associated with age (JT: cortex P < 0.001, cerebellum P < 0.001) (Figure 2D,F)
Summary
The mechanisms underlying central nervous system (CNS) dysfunction and cognitive deterioration during ageing are complex. The BBB is formed by a continuous layer of cerebral endothelial cells (CECs) held together by tight junctions, which limit paracellular and intramembranous diffusion. This restricts penetration of molecules into the CNS and provides high electrical resistance [1]. The phenotype of CECs is under inductive influence of perivascular pericytes and the end-feet of astrocytes Together, these cells form a functional cellular complex termed the ‘neurovascular unit’ (NVU), which provides a coordinated response to maintain CNS homeostasis and function [6]
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