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Journal articles on the topic 'White matter'

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Author: Grafiati
Published: 4 June 2021
Last updated: 22 June 2024

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1

Alkhatib, Ahed J. "WHITE MATTER ASSOCIATED DISEASES." Indian Research Journal of Pharmacy and Science 5, no. 2 (2018): 1416–19. http://dx.doi.org/10.21276/irjps.2018.5.2.2.

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2

Douglas Fields, R. "White Matter Matters." Scientific American 298, no. 3 (March 2008): 54–61. http://dx.doi.org/10.1038/scientificamerican0308-54.

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3

Mattson, Mark P. "Neurogenetics: white matter matters." Trends in Genetics 18, no. 2 (February 2002): 71. http://dx.doi.org/10.1016/s0168-9525(02)02627-6.

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4

Mattson, Mark P. "Neurogenetics: white matter matters." Trends in Neurosciences 25, no. 3 (March 2002): 135–36. http://dx.doi.org/10.1016/s0166-2236(02)02135-5.

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5

Xu, Man-Yu, Zhi-Qiang Xu, and Yan-Jiang Wang. "White Matter “Matters” in Alzheimer’s Disease." Neuroscience Bulletin 38, no. 3 (December 1, 2021): 323–26. http://dx.doi.org/10.1007/s12264-021-00803-8.

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6

Caixeta, Leonardo. "What matters in white matter dementia?" Dementia & Neuropsychologia 1, no. 2 (June 2007): 131–39. http://dx.doi.org/10.1590/s1980-57642008dn10200004.

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Abstract Dementia studies has primarily focused on disorders of the cerebral cortex and subcortical gray matter, what originated the concepts of cortical and subcortical dementias respectively. Dementia related mainly with cerebral white matter have received less attention. We present five different cases, each one illustrative of a dementia subtype that could be assigned under the category of 'white matter dementia': CADASIL, progressive subcortical gliosis, progressive multifocal leucoencephalopathy, normopressure hydrocephalus and brain injury. Besides that, recent clinical and scientific literature on white matter dementia was reviewed. The composition of exuberant psychiatric symptoms and personality changes (mainly apathy, but also desinhibition) with neurological signs (pyramidal alone or associated with extrapyramidal signs, ataxia and urinary incontinence) and with specific cognitive impairment (mentioned above), should rise strongly the possibility of a white-matter dementia, instead of a cortical or subcortical form of dementia.
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7

Hudson, Ann. "White Matter." Prairie Schooner 89, no. 2 (2015): 45–46. http://dx.doi.org/10.1353/psg.2015.0058.

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8

Dammann, Olaf, Scott Durum, and Alan Leviton. "Do white cells matter in white matter damage?" Trends in Neurosciences 24, no. 6 (June 2001): 320–24. http://dx.doi.org/10.1016/s0166-2236(00)01811-7.

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9

Crawford, Colin L. "Do white cells matter in white-matter damage?" Trends in Neurosciences 25, no. 1 (January 2002): 20–21. http://dx.doi.org/10.1016/s0166-2236(00)02064-6.

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10

Hamilton, Roy Hoshi, and Olga Ciccarelli. "Non-White Participants Matter in White Matter Disease Studies." Neurology 98, no. 9 (January 19, 2022): 345–46. http://dx.doi.org/10.1212/wnl.0000000000013224.

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11

Dammann, Olaf, Scott Durum, and Alan Leviton. "Response – Do white cells matter in white-matter damage?" Trends in Neurosciences 25, no. 1 (January 2002): 21. http://dx.doi.org/10.1016/s0166-2236(00)02065-8.

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12

Filley, Christopher M. "Cognition in cerebral palsy: White matter matters." European Journal of Paediatric Neurology 32 (May 2021): A1. http://dx.doi.org/10.1016/j.ejpn.2021.05.005.

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13

Zeffiro, Thomas, and Guinevere Eden. "What's the Matter? White Matter?" Neuron 25, no. 2 (February 2000): 257–59. http://dx.doi.org/10.1016/s0896-6273(00)80890-9.

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14

Yassi, Nawaf, and Bruce C. V. Campbell. "White Matter Hyperintensities." Neurology 96, no. 17 (March 16, 2021): 781–82. http://dx.doi.org/10.1212/wnl.0000000000011829.

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15

Millichap, J. Gordon. "White Matter Dementia." Pediatric Neurology Briefs 12, no. 7 (July 1, 1998): 55. http://dx.doi.org/10.15844/pedneurbriefs-12-7-11.

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16

Boyd, Herb. "White Lies Matter." James Baldwin Review 7, no. 1 (September 28, 2021): 184–96. http://dx.doi.org/10.7227/jbr.7.11.

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This review essay examines Eddie Glaude, Jr.’s new book Begin Again: James Baldwin’s America and Its Urgent Lessons for Our Own against several other recent works on Baldwin such as Bill Mullen’s James Baldwin: Living in Fire and Nicholas Buccola’s The Fire Is Upon Us.
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17

Schmahmann, Jeremy D., Eric E. Smith, Florian S. Eichler, and Christopher M. Filley. "Cerebral White Matter." Annals of the New York Academy of Sciences 1142, no. 1 (October 2008): 266–309. http://dx.doi.org/10.1196/annals.1444.017.

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18

Filley, Christopher M. "White matter dementia." Therapeutic Advances in Neurological Disorders 5, no. 5 (September 2012): 267–77. http://dx.doi.org/10.1177/1756285612454323.

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19

Lyoo, Kyoon, Itsuko Mino, Perry F. Renshaw, and Ho Kyu Lee. "WHITE MATTER HYPERINTENSITIES." Journal of the American Academy of Child & Adolescent Psychiatry 34, no. 7 (July 1995): 833–34. http://dx.doi.org/10.1097/00004583-199507000-00004.

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20

Filley, Christopher M. "Tracking white matter." Lancet Neurology 6, no. 1 (January 2007): 27. http://dx.doi.org/10.1016/s1474-4422(06)70674-3.

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21

Petty, Margaret A., and Joseph G. Wettstein. "White matter ischaemia." Brain Research Reviews 31, no. 1 (December 1999): 58–64. http://dx.doi.org/10.1016/s0165-0173(99)00025-9.

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22

Wycoco, Victor, Manohar Shroff, Sniya Sudhakar, and Wayne Lee. "White Matter Anatomy." Neuroimaging Clinics of North America 23, no. 2 (May 2013): 197–216. http://dx.doi.org/10.1016/j.nic.2012.12.002.

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23

Habes, Mohamad, Aristeidis Sotiras, Guray Erus, Jon B. Toledo, Deborah Janowitz, David A. Wolk, Haochang Shou, et al. "White matter lesions." Neurology 91, no. 10 (August 3, 2018): e964-e975. http://dx.doi.org/10.1212/wnl.0000000000006116.

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ObjectivesTo investigate spatial heterogeneity of white matter lesions or hyperintensities (WMH).MethodsMRI scans of 1,836 participants (median age 52.2 ± 13.16 years) encompassing a wide age range (22–84 years) from the cross-sectional Study of Health in Pomerania (Germany) were included as discovery set identifying spatially distinct components of WMH using a structural covariance approach. Scans of 307 participants (median age 73.8 ± 10.2 years, with 747 observations) from the Baltimore Longitudinal Study of Aging (United States) were included to examine differences in longitudinal progression of these components. The associations of these components with vascular risk factors, cortical atrophy, Alzheimer disease (AD) genetics, and cognition were then investigated using linear regression.ResultsWMH were found to occur nonuniformly, with higher frequency within spatially heterogeneous patterns encoded by 4 components, which were consistent with common categorizations of deep and periventricular WMH, while further dividing the latter into posterior, frontal, and dorsal components. Temporal trends of the components differed both cross-sectionally and longitudinally. Frontal periventricular WMH were most distinctive as they appeared in the fifth decade of life, whereas the other components appeared later in life during the sixth decade. Furthermore, frontal WMH were associated with systolic blood pressure and with pronounced atrophy including AD-related regions. AD polygenic risk score was associated with the dorsal periventricular component in the elderly. Cognitive decline was associated with the dorsal component.ConclusionsThese results support the hypothesis that the appearance of WMH follows age and disease-dependent regional distribution patterns, potentially influenced by differential underlying pathophysiologic mechanisms, and possibly with a differential link to vascular and neurodegenerative changes.
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24

Peckham, Haley. "White Matter Plasticity." Neuropsychotherapist, no. 4 (January 1, 2014): 98–99. http://dx.doi.org/10.12744/tnpt(4)098-099.

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25

Arkink, Enrico B., Inge H. Palm-Meinders, Hille Koppen, Julien Milles, Baldur van Lew, Lenore J. Launer, Paul A. M. Hofman, et al. "Microstructural white matter changes preceding white matter hyperintensities in migraine." Neurology 93, no. 7 (July 11, 2019): e688-e694. http://dx.doi.org/10.1212/wnl.0000000000007940.

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ObjectiveWe used magnetization transfer imaging to assess white matter tissue integrity in migraine, to explore whether white matter microstructure was more diffusely affected beyond visible white matter hyperintensities (WMHs), and to explore whether focal invisible microstructural changes precede visible focal WMHs in migraineurs.MethodsWe included 137 migraineurs (79 with aura, 58 without aura) and 74 controls from the Cerebral Abnormalities in Migraine, an Epidemiological Risk Analysis (CAMERA) study, a longitudinal population-based study on structural brain lesions in migraine patients, who were scanned at baseline and at a 9-year follow-up. To assess microstructural brain tissue integrity, baseline magnetization transfer ratio (MTR) values were calculated for whole brain white matter. Baseline MTR values were determined for areas of normal-appearing white matter (NAWM) that had progressed into MRI-detectable WMHs at follow-up and compared to MTR values of contralateral NAWM.ResultsMTR values for whole brain white matter did not differ between migraineurs and controls. In migraineurs, but not in controls, NAWM that later progressed to WMHs at follow-up had lower mean MTR (mean [SD] 0.354 [0.009] vs 0.356 [0.008], p = 0.047) at baseline as compared to contralateral white matter.ConclusionsWe did not find evidence for widespread microstructural white matter changes in migraineurs compared to controls. However, our findings suggest that a gradual or stepwise process might be responsible for evolution of focal invisible microstructural changes into focal migraine-related visible WMHs.
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26

Reginold, William, Kevin Sam, Julien Poublanc, Joe Fisher, Adrian Crawley, and David J. Mikulis. "Impact of white matter hyperintensities on surrounding white matter tracts." Neuroradiology 60, no. 9 (July 20, 2018): 933–44. http://dx.doi.org/10.1007/s00234-018-2053-x.

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27

Wang, Xiaoyang, and Carina Mallard. "Editorial: White blood cells matter in neonatal white-matter injury." Journal of Leukocyte Biology 99, no. 1 (January 2016): 4–6. http://dx.doi.org/10.1189/jlb.3ce0615-242r.

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28

Wu, Ruozhen, Jianlan Gu, Dingwei Zhou, Yunn Chyn Tung, Nana Jin, Dandan Chu, Wen Hu, et al. "Seeding-Competent Tau in Gray Matter Versus White Matter of Alzheimer’s Disease Brain." Journal of Alzheimer's Disease 79, no. 4 (February 16, 2021): 1647–59. http://dx.doi.org/10.3233/jad-201290.

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Background: Neurofibrillary pathology of abnormally hyperphosphorylated tau spreads along neuroanatomical connections, underlying the progression of Alzheimer’s disease (AD). The propagation of tau pathology to axonally connected brain regions inevitably involves trafficking of seeding-competent tau within the axonal compartment of the neuron. Objective: To determine the seeding activity of tau in cerebral gray and white matters of AD. Methods: Levels of total tau, hyperphosphorylation of tau, and SDS- and β-mercaptoethanol–resistant high molecular weight tau (HMW-tau) in crude extracts from gray and white matters of AD frontal lobes were analyzed by immuno-blots. Tau seeding activity was quantitatively assessed by measuring RIPA buffer–insoluble tau in HEK-293FT/tau151-391 cells treated with brain extracts. Results: We found a comparable level of soluble tau in gray matter versus white matter of control brains, but a higher level of soluble tau in gray matter than white matter of AD brains. In AD brains, tau is hyperphosphorylated in both gray and white matters, with a higher level in the former. The extracts of both gray and white matters of AD brains seeded tau aggregation in HEK-293FT/tau151–391 cells but the white matter showed less potency. Seeding activity of tau in brain extracts was positively correlated with the levels of tau hyperphosphorylation and HMW-tau. RIPA-insoluble tau, but not RIPA-soluble tau, was hyperphosphorylated tau at multiple sites. Conclusion: Both gray and white matters of AD brain contain seeding-competent tau that can template aggregation of hyperphosphorylated tau, but the seeding potency is markedly higher in gray matter than in white matter.
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29

Rinholm, J. E., and L. H. Bergersen. "White matter lactate – Does it matter?" Neuroscience 276 (September 2014): 109–16. http://dx.doi.org/10.1016/j.neuroscience.2013.10.002.

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30

Werner, Hauke B., and Olaf Jahn. "Myelin matters: proteomic insights into white matter disorders." Expert Review of Proteomics 7, no. 2 (April 2010): 159–64. http://dx.doi.org/10.1586/epr.09.105.

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31

Cronberg, Tobias. "White matter is what matters after cardiac arrest." Lancet Neurology 17, no. 4 (April 2018): 291–92. http://dx.doi.org/10.1016/s1474-4422(18)30079-6.

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32

Kong, Jiming, and Teng Guan. "Functional regeneration of the brain: white matter matters." Neural Regeneration Research 10, no. 3 (2015): 355. http://dx.doi.org/10.4103/1673-5374.153675.

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33

Silbert, L. C., D. B. Howieson, H. Dodge, and J. A. Kaye. "Cognitive impairment risk: White matter hyperintensity progression matters." Neurology 73, no. 2 (July 13, 2009): 120–25. http://dx.doi.org/10.1212/wnl.0b013e3181ad53fd.

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34

Kumar, Harish, Abhinav Gupta, Siddharth Savyasachi Malu, and Shashikant Gupta. "Slow Accretion of Helium Rich Matter onto C-O White Dwarf: Does Composition of WD Matter?" Indian Journal of Science and Technology 14, no. 44 (November 21, 2021): 3288–94. http://dx.doi.org/10.17485/ijst/v14i44.1681.

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35

Stys, Peter. "White Matter Injury Mechanisms." Current Molecular Medicine 4, no. 2 (March 1, 2004): 113–30. http://dx.doi.org/10.2174/1566524043479220.

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36

Tkach, Jean, Stephanie Merhar, and Beth Kline-Fath. "Premature white matter disease." Journal of Pediatric Neuroradiology 02, no. 01 (July 29, 2015): 017–32. http://dx.doi.org/10.3233/pnr-13044.

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37

Hofer, Edith, Margherita Cavalieri, Joshua C. Bis, Charles DeCarli, Myriam Fornage, Sigurdur Sigurdsson, Velandai Srikanth, et al. "White Matter Lesion Progression." Stroke 46, no. 11 (November 2015): 3048–57. http://dx.doi.org/10.1161/strokeaha.115.009252.

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38

Kruesi, M. J. P., and M. F. Casanova. "White matter in liars." British Journal of Psychiatry 188, no. 3 (March 2006): 293–94. http://dx.doi.org/10.1192/bjp.188.3.293-a.

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39

Lee, Phil Hyu, Oh Young Bang, Se Ho Oh, In Soo Joo, and Kyoon Huh. "Subcortical White Matter Infarcts." Stroke 34, no. 11 (November 2003): 2630–35. http://dx.doi.org/10.1161/01.str.0000097609.66185.05.

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40

Goldman, Steven A. "White matter from fibroblasts." Nature Biotechnology 31, no. 5 (May 2013): 412–13. http://dx.doi.org/10.1038/nbt.2570.

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41

Whalley, Katherine. "Understanding white matter defects." Nature Reviews Neuroscience 8, no. 6 (June 2007): 411. http://dx.doi.org/10.1038/nrn2162.

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42

Maillard, Pauline, Evan Fletcher, Danielle Harvey, Owen Carmichael, Bruce Reed, Dan Mungas, and Charles DeCarli. "White Matter Hyperintensity Penumbra." Stroke 42, no. 7 (July 2011): 1917–22. http://dx.doi.org/10.1161/strokeaha.110.609768.

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43

Deibert, Ellen, and Pashtun Shahim. "White matter and concussion." Neurology 95, no. 7 (July 8, 2020): 279–80. http://dx.doi.org/10.1212/wnl.0000000000009934.

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44

Wandell, Brian A. "Clarifying Human White Matter." Annual Review of Neuroscience 39, no. 1 (July 8, 2016): 103–28. http://dx.doi.org/10.1146/annurev-neuro-070815-013815.

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45

van der Knaap, Marjo S., Jan C. Pronk, and Gert C. Scheper. "Vanishing white matter disease." Lancet Neurology 5, no. 5 (May 2006): 413–23. http://dx.doi.org/10.1016/s1474-4422(06)70440-9.

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46

Karadottir, R. T., and K. B. Walhovd. "The CNS White Matter." Neuroscience 276 (September 2014): 1. http://dx.doi.org/10.1016/j.neuroscience.2014.03.010.

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47

Prange, H., and T. Weber. "„Vanishing white matter disease“." Der Nervenarzt 82, no. 10 (April 20, 2011): 1330–34. http://dx.doi.org/10.1007/s00115-011-3284-9.

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48

Zimmerman, R. A. "Inherited White Matter Diseases." Rivista di Neuroradiologia 19, no. 1 (February 2006): 37–41. http://dx.doi.org/10.1177/197140090601900105.

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49

Wallace, Carla J., and Robert J. Sevick. "Multifocal white matter lesions." Seminars in Ultrasound, CT and MRI 17, no. 3 (June 1996): 251–64. http://dx.doi.org/10.1016/s0887-2171(96)90038-4.

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50

Mori, Susumu, and Peter van Zijl. "Human White Matter Atlas." American Journal of Psychiatry 164, no. 7 (July 2007): 1005. http://dx.doi.org/10.1176/ajp.2007.164.7.1005.

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