Cited by 70Advanced Neuroimaging Techniques and ApplicationsCerebrovascular and genetic disordersNeuroscience and Neuropharmacology Research

Roles of white matter in central nervous system pathophysiologies

Open access
Matute, Carlos, Ransom, Bruce R·2012·ASN Neuro

Abstract

The phylogenetic enlargement of cerebral cortex culminating in the human brain imposed greater communication needs that have been met by the massive expansion of WM (white matter). Damage to WM alters brain function, and numerous neurological diseases feature WM involvement. In the current review, we discuss the major features of WM, the contributions of WM compromise to brain pathophysiology, and some of the mechanisms mediating WM injury. We will emphasize the newly appreciated importance of neurotransmitter signalling in WM, particularly glutamate and ATP signalling, to understanding both normal and abnormal brain functions. A deeper understanding of the mechanisms leading to WM damage will generate much-needed insights for developing therapies for acute and chronic diseases with WM involvement.

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Crossref · 10.1042/an20110060

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  • Loss of myelin slows axon potential transmission and threatens axon integrity, leading to axonal loss.

    “In addition to the brain dysfunction caused by slowing down the transmission of axon potentials, demyelination threatens the integrity of the axons and leads to axonal loss (Franklin and Ffrench-Constant, 2008; Matute and Ransom, 2012).”

    From The Pathobiology of Vascular Dementia (2013) · cites this paper as Matute and Ransom, 2012

  • Intracellular Na+ accumulation reverses the Na+/Ca2+ exchanger, causing intracellular Ca2+ accumulation.

    “The resulting accumulation of intracellular Na+ reverses the operation of the Na+/Ca2+ exchanger, resulting in intracellular Ca2+ accumulation (Matute and Ransom, 2012; Stys et al., 1992).”

    From The Pathobiology of Vascular Dementia (2013) · cites this paper as Matute and Ransom, 2012

  • Excess intracellular Ca2+ activates protease-dependent processes that fragment microtubules and perturb axonal flow.

    “In turn, excess intracellular Ca2+ activates protease dependent processes that lead to microtubule fragmentation and perturbation of axonal flow (Franklin and Ffrench-Constant, 2008; Matute and Ransom, 2012).”

    From The Pathobiology of Vascular Dementia (2013) · cites this paper as Matute and Ransom, 2012

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  1. Kettenmann H Ransom BR Neuroglia, Oxford University Press, Oxford. 2005

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Authors
Matute, C., & Ransom, B. R.
Affiliations
  • University of the Basque Country (ES)
  • University of Washington (US)
Corresponding author
Matute, Carlos
Venue
ASN Neuro
Published
2012-02
Volume
4
Issue
2
ISSN
1759-0914 (ISSN-L)
OpenAlex
W1991530671
Cited by
70
References
133
Citations by year
2026: 2 · 2025: 2 · 2024: 3 · 2023: 6 · 2022: 8 · 2021: 2 · 2020: 7 · 2019: 2 · 2018: 4 · 2017: 4 · 2016: 9 · 2015: 4 · 2014: 7 · 2013: 7 · 2012: 3
FWCI
0.90
Type
journal article
Language
en
Open access
Locations
  • ASN NEURO (publishedVersion, cc-by-nc)
  • PubMed Central (publishedVersion, cc-by-nc)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • Eusko Jaurlaritza
  • Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas
  • National Institutes of Health
Topics
  • Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Advanced Neuroimaging Techniques and Applications
  • Health Sciences › Medicine › Neurology › Cerebrovascular and genetic disorders
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Keywords
white matter, white matter injury, glutamate signalling, ATP signalling, neurotransmitter signalling, neurological disorders, brain injury mechanisms, cerebral cortex evolution
MeSH terms
Adenosine Triphosphate, Animals, Axons, Central Nervous System Diseases, Humans, Nerve Fibers, Myelinated, Neuroglia, Signal Transduction, Neurotransmitter Agents, Glutamic Acid

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