Articles de revues : « White matter maturation »

1

Millichap, J. Gordon. « White Matter Maturation in Holoprosencephaly ». Pediatric Neurology Briefs 17, n^o 1 (1 janvier 2003) : 2. http://dx.doi.org/10.15844/pedneurbriefs-17-1-2.

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Yu, Qinlin, Yun Peng, Huiying Kang, Qinmu Peng, Minhui Ouyang, Michelle Slinger, Di Hu, Haochang Shou, Fang Fang et Hao Huang. « Differential White Matter Maturation from Birth to 8 Years of Age ». Cerebral Cortex 30, n^o 4 (9 décembre 2019) : 2674–90. http://dx.doi.org/10.1093/cercor/bhz268.

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Abstract Comprehensive delineation of white matter (WM) microstructural maturation from birth to childhood is critical for understanding spatiotemporally differential circuit formation. Without a relatively large sample of datasets and coverage of critical developmental periods of both infancy and early childhood, differential maturational charts across WM tracts cannot be delineated. With diffusion tensor imaging (DTI) of 118 typically developing (TD) children aged 0–8 years and 31 children with autistic spectrum disorder (ASD) aged 2–7 years, the microstructure of every major WM tract and tract group was measured with DTI metrics to delineate differential WM maturation. The exponential model of microstructural maturation of all WM was identified. The WM developmental curves were separated into fast, intermediate, and slow phases in 0–8 years with distinctive time period of each phase across the tracts. Shorter periods of the fast and intermediate phases in certain tracts, such as the commissural tracts, indicated faster earlier development. With TD WM maturational curves as the reference, higher residual variance of WM microstructure was found in children with ASD. The presented comprehensive and differential charts of TD WM microstructural maturation of all major tracts and tract groups in 0–8 years provide reference standards for biomarker detection of neuropsychiatric disorders.

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Bugiani, Marianna, Ilja Boor, Barbara van Kollenburg, Nienke Postma, Emiel Polder, Carola van Berkel, Ronald E. van Kesteren et al. « Defective Glial Maturation in Vanishing White Matter Disease ». Journal of Neuropathology & ; Experimental Neurology 70, n^o 1 (janvier 2011) : 69–82. http://dx.doi.org/10.1097/nen.0b013e318203ae74.

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Bells, Sonya, Jérémie Lefebvre, Giulia Longoni, Sridar Narayanan, Douglas L. Arnold, Eleun Ann Yeh et Donald J. Mabbott. « White matter plasticity and maturation in human cognition ». Glia 67, n^o 11 (24 juin 2019) : 2020–37. http://dx.doi.org/10.1002/glia.23661.

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Bava, Sunita, Rachel Thayer, Joanna Jacobus, Megan Ward, Terry L. Jernigan et Susan F. Tapert. « Longitudinal characterization of white matter maturation during adolescence ». Brain Research 1327 (avril 2010) : 38–46. http://dx.doi.org/10.1016/j.brainres.2010.02.066.

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Kulikova, S., L. Hertz-Pannier, G. Dehaene-Lambertz, A. Buzmakov, C. Poupon et J. Dubois. « Multi-parametric evaluation of the white matter maturation ». Brain Structure and Function 220, n^o 6 (3 septembre 2014) : 3657–72. http://dx.doi.org/10.1007/s00429-014-0881-y.

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Herting, Megan M., Robert Kim, Kristina A. Uban, Eric Kan, Andrea Binley et Elizabeth R. Sowell. « Longitudinal changes in pubertal maturation and white matter microstructure ». Psychoneuroendocrinology 81 (juillet 2017) : 70–79. http://dx.doi.org/10.1016/j.psyneuen.2017.03.017.

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Barkovich, A. J., E. M. Simon, O. A. Glenn, N. J. Clegg, S. L. Kinsman, M. Delgado et J. S. Hahn. « MRI shows abnormal white matter maturation in classical holoprosencephaly ». Neurology 59, n^o 12 (24 décembre 2002) : 1968–71. http://dx.doi.org/10.1212/01.wnl.0000038354.10891.0e.

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Kansagra, Akash P., Marc C. Mabray, Donna M. Ferriero, A. James Barkovich, Duan Xu et Christopher P. Hess. « Microstructural maturation of white matter tracts in encephalopathic neonates ». Clinical Imaging 40, n^o 5 (septembre 2016) : 1009–13. http://dx.doi.org/10.1016/j.clinimag.2016.05.009.

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Scantlebury, Nadia, Todd Cunningham, Colleen Dockstader, Suzanne Laughlin, William Gaetz, Conrad Rockel, Jolynn Dickson et Donald Mabbott. « Relations between White Matter Maturation and Reaction Time in Childhood ». Journal of the International Neuropsychological Society 20, n^o 1 (29 octobre 2013) : 99–112. http://dx.doi.org/10.1017/s1355617713001148.

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AbstractWhite matter matures with age and is important for the efficient transmission of neuronal signals. Consequently, white matter growth may underlie the development of cognitive processes important for learning, including the speed of information processing. To dissect the relationship between white matter structure and information processing speed, we administered a reaction time task (finger abduction in response to visual cue) to 27 typically developing, right-handed children aged 4 to 13. Magnetoencephalography and Diffusion Tensor Imaging were used to delineate white matter connections implicated in visual-motor information processing. Fractional anisotropy (FA) and radial diffusivity (RD) of the optic radiation in the left hemisphere, and FA and mean diffusivity (MD) of the optic radiation in the right hemisphere changed significantly with age. MD and RD decreased with age in the right inferior fronto-occipital fasciculus, and bilaterally in the cortico-spinal tracts. No age-related changes were evident in the inferior longitudinal fasciculus. FA of the cortico-spinal tract in the left hemisphere and MD of the inferior fronto-occipital fasciculus of the right hemisphere contributed uniquely beyond the effect of age in accounting for reaction time performance of the right hand. Our findings support the role of white matter maturation in the development of information processing speed. (JINS, 2013, 19, 1–14)

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Wilson, Siân, Maximilian Pietsch, Lucilio Cordero-Grande, Anthony N. Price, Jana Hutter, Jiaxin Xiao, Laura McCabe et al. « Development of human white matter pathways in utero over the second and third trimester ». Proceedings of the National Academy of Sciences 118, n^o 20 (10 mai 2021) : e2023598118. http://dx.doi.org/10.1073/pnas.2023598118.

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During the second and third trimesters of human gestation, rapid neurodevelopment is underpinned by fundamental processes including neuronal migration, cellular organization, cortical layering, and myelination. In this time, white matter growth and maturation lay the foundation for an efficient network of structural connections. Detailed knowledge about this developmental trajectory in the healthy human fetal brain is limited, in part, due to the inherent challenges of acquiring high-quality MRI data from this population. Here, we use state-of-the-art high-resolution multishell motion-corrected diffusion-weighted MRI (dMRI), collected as part of the developing Human Connectome Project (dHCP), to characterize the in utero maturation of white matter microstructure in 113 fetuses aged 22 to 37 wk gestation. We define five major white matter bundles and characterize their microstructural features using both traditional diffusion tensor and multishell multitissue models. We found unique maturational trends in thalamocortical fibers compared with association tracts and identified different maturational trends within specific sections of the corpus callosum. While linear maturational increases in fractional anisotropy were seen in the splenium of the corpus callosum, complex nonlinear trends were seen in the majority of other white matter tracts, with an initial decrease in fractional anisotropy in early gestation followed by a later increase. The latter is of particular interest as it differs markedly from the trends previously described in ex utero preterm infants, suggesting that this normative fetal data can provide significant insights into the abnormalities in connectivity which underlie the neurodevelopmental impairments associated with preterm birth.

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Hubl, D., V. Chauvin, M. Zeller, A. Federspiel, C. Boesch, W. Strik, T. Dierks et T. Koenig. « 226 – Evidence for white matter maturation impairment in auditory hallucinations ». Schizophrenia Research 98 (février 2008) : 126–27. http://dx.doi.org/10.1016/j.schres.2007.12.293.

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Back, Stephen A., Art Riddle et Melissa M. McClure. « Maturation-Dependent Vulnerability of Perinatal White Matter in Premature Birth ». Stroke 38, n^o 2 (février 2007) : 724–30. http://dx.doi.org/10.1161/01.str.0000254729.27386.05.

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Segovia, Kristen N., Melissa McClure, Matthew Moravec, Ning Ling Luo, Ying Wan, Xi Gong, Art Riddle et al. « Arrested oligodendrocyte lineage maturation in chronic perinatal white matter injury ». Annals of Neurology 63, n^o 4 (avril 2008) : 520–30. http://dx.doi.org/10.1002/ana.21359.

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Friedrichs-Maeder, Cecilia L., Alessandra Griffa, Juliane Schneider, Petra Susan Hüppi, Anita Truttmann et Patric Hagmann. « Exploring the role of white matter connectivity in cortex maturation ». PLOS ONE 12, n^o 5 (17 mai 2017) : e0177466. http://dx.doi.org/10.1371/journal.pone.0177466.

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Hesselink, John R. « Myelin Maturation and White Matter Development : An Embryologic Eye View ». Neuroradiology Journal 22, n^o 1_suppl (septembre 2009) : 11–17. http://dx.doi.org/10.1177/19714009090220s104.

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Blüml, Stefan, Jessica L. Wisnowski, Marvin D. Nelson, Lisa Paquette et Ashok Panigrahy. « Metabolic Maturation of White Matter Is Altered in Preterm Infants ». PLoS ONE 9, n^o 1 (22 janvier 2014) : e85829. http://dx.doi.org/10.1371/journal.pone.0085829.

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Baierl, P., Ch Förster, H. Fendel, M. Naegele, U. Fink et W. Kenn. « Magnetic resonance imaging of normal and pathological white matter maturation ». Pediatric Radiology 18, n^o 3 (avril 1988) : 183–89. http://dx.doi.org/10.1007/bf02390391.

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Ranade, S. S., P. N. Trivedi et V. S. Bamane. « Magnetic resonance imaging of normal and pathological white matter maturation ». Pediatric Radiology 19, n^o 5 (juin 1989) : 346. http://dx.doi.org/10.1007/bf02467314.

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Nagy, Zoltan, Helena Westerberg et Torkel Klingberg. « Maturation of White Matter is Associated with the Development of Cognitive Functions during Childhood ». Journal of Cognitive Neuroscience 16, n^o 7 (septembre 2004) : 1227–33. http://dx.doi.org/10.1162/0898929041920441.

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In the human brain, myelination of axons continues until early adulthood and is thought to be important for the development of cognitive functions during childhood. We used diffusion tensor MR imaging and calculated fractional anisotropy, an indicator of myelination and axonal thickness, in children aged between 8 and 18 years. Development of working memory capacity was positively correlated with fractional anisotropy in two regions in the left frontal lobe, including a region between the superior frontal and parietal cortices. Reading ability, on the other hand, was only correlated with fractional anisotropy in the left temporal lobe, in the same white matter region where adults with reading disability are known to have lower fractional anisotropy. Both the temporal and the frontal regions were also correlated with age. These results show that maturation of white matter is an important part of brain maturation during childhood, and that maturation of relatively restricted regions of white matter is correlated with development of specific cognitive functions.

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Gerstner, B., T. M. DeSilva, K. Genz, A. Armstrong, F. Brehmer, R. L. Neve, U. Felderhoff-Mueser, J. J. Volpe et P. A. Rosenberg. « Hyperoxia Causes Maturation-Dependent Cell Death in the Developing White Matter ». Journal of Neuroscience 28, n^o 5 (30 janvier 2008) : 1236–45. http://dx.doi.org/10.1523/jneurosci.3213-07.2008.

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Olivier, Paul, Romain H. Fontaine, Gauthier Loron, Juliette Van Steenwinckel, Valérie Biran, Véronique Massonneau, Angela Kaindl et al. « Melatonin Promotes Oligodendroglial Maturation of Injured White Matter in Neonatal Rats ». PLoS ONE 4, n^o 9 (22 septembre 2009) : e7128. http://dx.doi.org/10.1371/journal.pone.0007128.

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Deoni, Sean C. L., Jonathan O’Muircheartaigh, Jed T. Elison, Lindsay Walker, Ellen Doernberg, Nicole Waskiewicz, Holly Dirks, Irene Piryatinsky, Doug C. Dean et N. L. Jumbe. « White matter maturation profiles through early childhood predict general cognitive ability ». Brain Structure and Function 221, n^o 2 (29 novembre 2014) : 1189–203. http://dx.doi.org/10.1007/s00429-014-0947-x.

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Moon, Won-Jin, James M. Provenzale, Basar Sarikaya, Yon Kwon Ihn, John Morlese, Steven Chen et Michael D. DeBellis. « Diffusion-Tensor Imaging Assessment of White Matter Maturation in Childhood and Adolescence ». American Journal of Roentgenology 197, n^o 3 (septembre 2011) : 704–12. http://dx.doi.org/10.2214/ajr.10.6382.

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Sung, Mi Sook, Ok Hwa Kim, Jung Lim Moon, Kyung Sub Shinn et Yong Whee Bahk. « Brain MRI in children with delayed development : emphasis on white matter maturation ». Journal of the Korean Radiological Society 28, n^o 3 (1992) : 457. http://dx.doi.org/10.3348/jkrs.1992.28.3.457.

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Bugiani, Marianna, Nienke Postma, Emiel Polder, Nikki Dieleman, Peter G. Scheffer, Fraser J. Sim, Marjo S. van der Knaap et Ilja Boor. « Hyaluronan accumulation and arrested oligodendrocyte progenitor maturation in vanishing white matter disease ». Brain 136, n^o 1 (janvier 2013) : 209–22. http://dx.doi.org/10.1093/brain/aws320.

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Hagmann, P., O. Sporns, N. Madan, L. Cammoun, R. Pienaar, V. J. Wedeen, R. Meuli, J. P. Thiran et P. E. Grant. « White matter maturation reshapes structural connectivity in the late developing human brain ». Proceedings of the National Academy of Sciences 107, n^o 44 (18 octobre 2010) : 19067–72. http://dx.doi.org/10.1073/pnas.1009073107.

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Glass, Torin J. A., Vann Chau, Jane Gardiner, Justin Foong, Jillian Vinall, Jill G. Zwicker, Ruth E. Grunau, Anne Synnes, Kenneth J. Poskitt et Steven P. Miller. « Severe retinopathy of prematurity predicts delayed white matter maturation and poorer neurodevelopment ». Archives of Disease in Childhood - Fetal and Neonatal Edition 102, n^o 6 (23 mai 2017) : F532—F537. http://dx.doi.org/10.1136/archdischild-2016-312533.

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Dai, Xiongtao, Pantelis Hadjipantelis, Jane‐Ling Wang, Sean C. L. Deoni et Hans‐Georg Müller. « Longitudinal associations between white matter maturation and cognitive development across early childhood ». Human Brain Mapping 40, n^o 14 (12 juin 2019) : 4130–45. http://dx.doi.org/10.1002/hbm.24690.

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Geeraert, Bryce L., Robert Marc Lebel et Catherine Lebel. « A multiparametric analysis of white matter maturation during late childhood and adolescence ». Human Brain Mapping 40, n^o 15 (7 juillet 2019) : 4345–56. http://dx.doi.org/10.1002/hbm.24706.

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Lepomäki, Virva, Marika Leppänen, Jaakko Matomäki, Helena Lapinleimu, Liisa Lehtonen, Leena Haataja, Markku Komu, Päivi Rautava et Riitta Parkkola. « Preterm infants’ early growth and brain white matter maturation at term age ». Pediatric Radiology 43, n^o 10 (23 juin 2013) : 1357–64. http://dx.doi.org/10.1007/s00247-013-2699-9.

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Bugiani, Marianna, Nienke Postma, Emiel Polder, Nikki Dieleman, Peter G. Scheffer, Fraser J. Sim, Marjo S. van der Knaap et Ilja Boor. « Hyaluronan accumulation and arrested oligodendrocyte progenitor maturation in Vanishing White Matter disease ». Tijdschrift voor Kindergeneeskunde 81, S1 (février 2013) : 28. http://dx.doi.org/10.1007/s12456-013-0028-8.

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Drobyshevsky, Alexander, Rugang Jiang, Matthew Derrick, Kehuan Luo et Sidhartha Tan. « Functional correlates of central white matter maturation in perinatal period in rabbits ». Experimental Neurology 261 (novembre 2014) : 76–86. http://dx.doi.org/10.1016/j.expneurol.2014.06.021.

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Geng, Xiujuan, Elizabeth C. Prom-Wormley, Javier Perez, Thomas Kubarych, Martin Styner, Weili Lin, Michael C. Neale et John H. Gilmore. « White Matter Heritability Using Diffusion Tensor Imaging in Neonatal Brains ». Twin Research and Human Genetics 15, n^o 3 (juin 2012) : 336–50. http://dx.doi.org/10.1017/thg.2012.14.

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Understanding genetic and environmental effects on white matter development in the first years of life is of great interest, as it provides insights into the etiology of neurodevelopmental disorders. In this study, the genetic and environmental effects on white matter were estimated using data from 173 neonatal twin subjects. Diffusion tensor imaging scans were acquired around 40 days after birth and were non-rigidly registered to a group-specific atlas and parcellated into 98 ROIs. A model of additive genetic, and common and specific environmental variance components was used to estimate overall and regional genetic and environmental contributions to diffusion parameters of fractional anisotropy, radial diffusivity, and axial diffusivity. Correlations between the regional heritability values and diffusion parameters were also examined. Results indicate that individual differences in overall white matter microstructure, represented by the average diffusion parameters over the whole brain, are heritable, and estimates are higher than found in studies in adults. Estimates of genetic and environmental variance components vary considerably across different white matter regions. Significant positive correlations between radial diffusivity heritability and radial diffusivity values are consistent with regional genetic variation being modulated by maturation status in the neonatal brain: the more mature the region is, the less genetic variation it shows. Common environmental effects are present in a few regions that tend to be characterized by low radial diffusivity. Results from the joint diffusion parameter analysis suggest that multivariate modeling approaches might be promising to better estimate maturation status and its relationship with genetic and environmental effects.

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van den Heuij, Lotte G., Mhoyra Fraser, Suzanne L. Miller, Graham Jenkin, Euan M. Wallace, Joanne O. Davidson, Christopher A. Lear et al. « Delayed intranasal infusion of human amnion epithelial cells improves white matter maturation after asphyxia in preterm fetal sheep ». Journal of Cerebral Blood Flow & ; Metabolism 39, n^o 2 (12 septembre 2017) : 223–39. http://dx.doi.org/10.1177/0271678x17729954.

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Perinatal hypoxic-ischemic (HI) brain injury remains highly associated with neurodevelopmental disability after preterm birth. There is increasing evidence that disability is linked with impaired white matter maturation, but there is no specific treatment. In this study, we evaluated whether, in preterm fetal sheep, delayed intranasal infusion of human amnion epithelial cells (hAECs) given 1, 3 and 10 days after severe HI, induced by umbilical cord occlusion for 25 min, can restore white matter maturation or reduce delayed cell loss. After 21 days recovery, asphyxia was associated with reduced electroencephalographic (EEG) maturation, brain weight and cortical area, impaired maturation of oligodendrocytes (OLs), no significant loss of total OLs but a marked reduction in immature/mature OLs and reduced myelination. Intranasal infusion of hAECs was associated with improved brain weight and restoration of immature/mature OLs and fractional area of myelin basic protein, with reduced microglia and astrogliosis. Cortical EEG frequency distribution was partially improved, with reduced loss of cortical area, and attenuated cleaved-caspase-3 expression and microgliosis. Neuronal survival in deep grey matter nuclei was improved, with reduced microglia, astrogliosis and cleaved-caspase-3-positive apoptosis. These findings suggest that delayed intranasal hAEC administration has potential to alleviate chronic dysmaturation after perinatal HI.

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Croteau-Chonka, Elise C., Douglas C. Dean, Justin Remer, Holly Dirks, Jonathan O'Muircheartaigh et Sean C. L. Deoni. « Examining the relationships between cortical maturation and white matter myelination throughout early childhood ». NeuroImage 125 (janvier 2016) : 413–21. http://dx.doi.org/10.1016/j.neuroimage.2015.10.038.

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Smyser, Tara A., Christopher D. Smyser, Cynthia E. Rogers, Sarah K. Gillespie, Terrie E. Inder et Jeffrey J. Neil. « Cortical Gray and Adjacent White Matter Demonstrate Synchronous Maturation in Very Preterm Infants ». Cerebral Cortex 26, n^o 8 (24 juillet 2015) : 3370–78. http://dx.doi.org/10.1093/cercor/bhv164.

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Monin, A., P. S. Baumann, A. Griffa, L. Xin, R. Mekle, M. Fournier, C. Butticaz et al. « Glutathione deficit impairs myelin maturation : relevance for white matter integrity in schizophrenia patients ». Molecular Psychiatry 20, n^o 7 (26 août 2014) : 827–38. http://dx.doi.org/10.1038/mp.2014.88.

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Maki, T., Y. K. Choi, N. Miyamoto, A. Shindo, S. Kaji, R. Takahashi, E. Lo et K. Arai. « A-kinase anchor protein 12 is indispensable for oligodendrocyte maturation in white matter ». Journal of the Neurological Sciences 381 (octobre 2017) : 842. http://dx.doi.org/10.1016/j.jns.2017.08.2370.

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Shiow, Lawrence R., Geraldine Favrais, Lucas Schirmer, Anne-Laure Schang, Sara Cipriani, Christian Andres, Jaclyn N. Wright et al. « Reactive astrocyte COX2-PGE2 production inhibits oligodendrocyte maturation in neonatal white matter injury ». Glia 65, n^o 12 (30 août 2017) : 2024–37. http://dx.doi.org/10.1002/glia.23212.

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Karlsson, Hasse, Harri Merisaari, Linnea Karlsson, Noora M. Scheinin, Riitta Parkkola, Jani Saunavaara, Tuire Lähdesmäki et al. « Association of Cumulative Paternal Early Life Stress With White Matter Maturation in Newborns ». JAMA Network Open 3, n^o 11 (24 novembre 2020) : e2024832. http://dx.doi.org/10.1001/jamanetworkopen.2020.24832.

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Birca, A., VA Vakorin, S. Madathil, V. Chau, SP Miller, SM Doesburg, M. Seed et al. « Interplay between impaired brain structure and function in term newborns with congenital heart disease ». Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 42, S1 (mai 2015) : S13—S14. http://dx.doi.org/10.1017/cjn.2015.85.

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Background: Term neonates with congenital heart disease (CHD) demonstrate a high incidence of white matter injury (WMI), together with increased average diffusivity and decreased fractional anisotropy (FA) on MR diffusion tensor imaging. EEG background activity is a robust measure of functional brain maturation that becomes less discontinuous, contains more fast activity and shows higher complexity of EEG patterns with increasing age. We sought to determine the association between structural brain abnormalities and functional brain maturation in term neonates with CHD. Methods: Thirteen term newborns with CHD underwent pre-operative MR imaging and continuous EEG recordings (cEEG). The proportion of cEEG with discontinuous vs. continuous background activity was quantified by visual analysis. During continuous epochs, we differentiated between two states: wakefulness/active sleep vs. quiet/transitional sleep, and applied algorithms to measure spectral power and EEG complexity. Results: Three patients had multifocal WMI which was associated with greater EEG background discontinuity (P<0.05). Moreover, lower white matter diffusivity was associated with higher power of fast activity (P<0.05 for wakefulness/active sleep EEG pattern), while higher white matter FA showed a trend toward being associated with increased EEG complexity (P<0.1 for quiet/transitional sleep pattern). Conclusions: In this series of term neonates with CHD, structural and microstructural white matter abnormalities are associated with impaired maturation of brain function.

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Sozmen, Elif G., Shira Rosenzweig, Irene L. Llorente, David J. DiTullio, Michal Machnicki, Harry V. Vinters, Lief A. Havton, Roman J. Giger, Jason D. Hinman et S. Thomas Carmichael. « Nogo receptor blockade overcomes remyelination failure after white matter stroke and stimulates functional recovery in aged mice ». Proceedings of the National Academy of Sciences 113, n^o 52 (12 décembre 2016) : E8453—E8462. http://dx.doi.org/10.1073/pnas.1615322113.

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White matter stroke is a distinct stroke subtype, accounting for up to 25% of stroke and constituting the second leading cause of dementia. The biology of possible tissue repair after white matter stroke has not been determined. In a mouse stroke model, white matter ischemia causes focal damage and adjacent areas of axonal myelin disruption and gliosis. In these areas of only partial damage, local white matter progenitors respond to injury, as oligodendrocyte progenitors (OPCs) proliferate. However, OPCs fail to mature into oligodendrocytes (OLs) even in regions of demyelination with intact axons and instead divert into an astrocytic fate. Local axonal sprouting occurs, producing an increase in unmyelinated fibers in the corpus callosum. The OPC maturation block after white matter stroke is in part mediated via Nogo receptor 1 (NgR1) signaling. In both aged and young adult mice, stroke induces NgR1 ligands and down-regulates NgR1 inhibitors during the peak OPC maturation block. Nogo ligands are also induced adjacent to human white matter stroke in humans. A Nogo signaling blockade with an NgR1 antagonist administered after stroke reduces the OPC astrocytic transformation and improves poststroke oligodendrogenesis in mice. Notably, increased white matter repair in aged mice is translated into significant poststroke motor recovery, even when NgR1 blockade is provided during the chronic time points of injury. These data provide a perspective on the role of NgR1 ligand function in OPC fate in the context of a specific and common type of stroke and show that it is amenable to systemic intervention to promote recovery.

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Provenzale, James M., Luxia Liang, David DeLong et Leonard E. White. « Diffusion Tensor Imaging Assessment of Brain White Matter Maturation During the First Postnatal Year ». American Journal of Roentgenology 189, n^o 2 (août 2007) : 476–86. http://dx.doi.org/10.2214/ajr.07.2132.

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Paus, T., D. L. Collins, A. C. Evans, G. Leonard, B. Pike et A. Zijdenbos. « Maturation of white matter in the human brain : a review of magnetic resonance studies ». Brain Research Bulletin 54, n^o 3 (février 2001) : 255–66. http://dx.doi.org/10.1016/s0361-9230(00)00434-2.

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Chang, Yi Shin, Julia P. Owen, Nicholas J. Pojman, Tony Thieu, Polina Bukshpun, Mari L. J. Wakahiro, Jeffrey I. Berman et al. « White Matter Changes of Neurite Density and Fiber Orientation Dispersion during Human Brain Maturation ». PLOS ONE 10, n^o 6 (26 juin 2015) : e0123656. http://dx.doi.org/10.1371/journal.pone.0123656.

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Krakauer, K., M. Nordentoft, B. Y. Glenthøj, J. M. Raghava, D. Nordholm, L. Randers, L. B. Glenthøj, B. H. Ebdrup et E. Rostrup. « White matter maturation during 12 months in individuals at ultra-high-risk for psychosis ». Acta Psychiatrica Scandinavica 137, n^o 1 (16 novembre 2017) : 65–78. http://dx.doi.org/10.1111/acps.12835.

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Lee, Ah Young, Sung Ho Jang, Eunsil Lee, Sang Ho Ahn, Hee Kyung Cho, Hae Min Jo et Su Min Son. « Radiologic differences in white matter maturation between preterm and full-term infants : TBSS study ». Pediatric Radiology 43, n^o 5 (13 novembre 2012) : 612–19. http://dx.doi.org/10.1007/s00247-012-2545-5.

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Groteklaes, Anne, Carina Bönisch, Britta Eiberger, Andrea Christ et Karl Schilling. « Developmental Maturation of the Cerebellar White Matter—an Instructive Environment for Cerebellar Inhibitory Interneurons ». Cerebellum 19, n^o 2 (30 janvier 2020) : 286–308. http://dx.doi.org/10.1007/s12311-020-01111-z.

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Grant, P. Ellen, Kiho Im, Banu Ahtam, Cynthia T. Laurentys, Wai-Man Chan, Maya Brainard, Sheena Chew et al. « Altered White Matter Organization in the TUBB3 E410K Syndrome ». Cerebral Cortex 29, n^o 8 (1 octobre 2018) : 3561–76. http://dx.doi.org/10.1093/cercor/bhy231.

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Abstract Seven unrelated individuals (four pediatric, three adults) with the TUBB3 E410K syndrome, harboring identical de novo heterozygous TUBB3 c.1228 G>A mutations, underwent neuropsychological testing and neuroimaging. Despite the absence of cortical malformations, they have intellectual and social disabilities. To search for potential etiologies for these deficits, we compared their brain's structural and white matter organization to 22 controls using structural and diffusion magnetic resonance imaging. Diffusion images were processed to calculate fractional anisotropy (FA) and perform tract reconstructions. Cortical parcellation-based network analysis and gyral topology-based FA analyses were performed. Major interhemispheric, projection and intrahemispheric tracts were manually segmented. Subjects had decreased corpus callosum volume and decreased network efficiency. While only pediatric subjects had diffuse decreases in FA predominantly affecting mid- and long-range tracts, only adult subjects had white matter volume loss associated with decreased cortical surface area. All subjects showed aberrant corticospinal tract trajectory and bilateral absence of the dorsal language network long segment. Furthermore, pediatric subjects had more tracts with decreased FA compared with controls than did adult subjects. These findings define a TUBB3 E410K neuroimaging endophenotype and lead to the hypothesis that the age-related changes are due to microscopic intrahemispheric misguided axons that are pruned during maturation.

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