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Cited by 239Barrier Structure and Function StudiesAmyotrophic Lateral Sclerosis ResearchIon Transport and Channel Regulation

Ultrastructure of blood–brain barrier and blood–spinal cord barrier in SOD1 mice modeling ALS

Garbuzova-Davis, Svitlana, Haller, Edward, Saporta, Samuel, Kolomey, Irina, Nicosia, Santo V., Sanberg, Paul R.·2007·Brain Research
DOI 10.1016/j.brainres.2007.04.044
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Abstract

The purpose of this study was to determine the ultrastructure of the blood-brain barrier (BBB) and blood-spinal cord barrier (BSCB) in G93A SOD1 mice modeling ALS at different stages of disease. Electron microscope examination of brainstem, cervical and lumbar spinal cords was performed in ALS mice at early and late stages of disease. Our results show disorganized mitochondrial cristae and degenerating mitochondria in endothelial cells and neuropil, swollen astrocyte foot processes, swollen and degenerating capillary endothelial cells, astrocytes and motor neurons and extensive extracellular edema. In spite of progressive extracellular edema in neural tissue, capillary endothelial cell tight junctions appeared to remain intact in early and late symptomatic animals. Results show that disruption of BBB and BSCB was evident in areas of motor neuron degeneration in G93A mice at both early and late stages of disease. Capillary rupture was observed in brainstem in early symptomatic G93A mice. Capillary ultrastructure revealed that endothelial cell membrane and/or basement membrane damage occurred, followed by vascular leakage.

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Crossref · 10.1016/j.brainres.2007.04.044

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  • Studies in SOD1 transgenic mice expressing dismutase-active (G93A and G37R) and dismutase-inactive (G85R) mutations have suggested that BSCB breakdown occurs before motor neuron injury.

    “Studies in SOD1 transgenic mice expressing dismutase-active (G93A and G37R) and dismutase-inactive (G85R) mutations have suggested that BSCB breakdown occurs before motor neuron injury (194, 415, 651, 687, 688).”

    From Blood-Brain Barrier: From Physiology to Disease and Back (2019) · cites this paper as [194]

  • SOD1 G93A mice develop ultrastructural capillary alterations, extravasation of red blood cells, and deposition of fibrin(ogen) and hemosiderin deposits in the brain stem and spinal cord early in the disease.

    “For instance, SOD1 G93A mice develop ultrastructural capillary alterations, extravasation of RBCs, and deposition of fibrin(ogen) and hemosiderin deposits in the brain stem and spinal cord early in the disease (194, 651, 687).”

    From Blood-Brain Barrier: From Physiology to Disease and Back (2019) · cites this paper as [194]

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Authors
Garbuzova-Davis, S., Haller, E., Saporta, S., Kolomey, I., Nicosia, S. V., & Sanberg, P. R.
Affiliations
University of South Florida (US)
ORCID
Venue
Brain Research
Publisher
Elsevier BV
Published
2007-07
Volume
1157
Pages
126-137
ISSN
0006-8993 (ISSN-L)
DOI
10.1016/j.brainres.2007.04.044
OpenAlex
W2091721686
Cited by
239
References
3
Citations by year
2026: 7 · 2025: 15 · 2024: 21 · 2023: 9 · 2022: 13 · 2021: 18 · 2020: 11 · 2019: 11 · 2018: 12 · 2017: 14 · 2016: 5 · 2015: 12 · 2014: 15 · 2013: 5 · 2012: 19
FWCI
8.51
Type
journal article
Language
en
Open access
closed
Licence
Locations
  • Brain Research (publishedVersion)
  • PubMed (publishedVersion)
  • Digital Commons - University of South Florida (University of South Florida) (submittedVersion)
Funders
University of San Francisco
Topics
  • Life Sciences › Neuroscience › Neurology › Barrier Structure and Function Studies
  • Health Sciences › Medicine › Neurology › Amyotrophic Lateral Sclerosis Research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion Transport and Channel Regulation
Keywords
blood-brain barrier, blood-spinal cord barrier, amyotrophic lateral sclerosis, SOD1 G93A mice, endothelial ultrastructure, mitochondrial cristae, motor neuron degeneration, extracellular edema, tight junctions, capillary rupture, vascular leakage, basement membrane damage, disease stage
MeSH terms
Superoxide Dismutase-1, Amyotrophic Lateral Sclerosis, Animals, Astrocytes, Basement Membrane, Blood-Brain Barrier, Brain, Brain Edema, Capillaries, Disease Models, Animal, Extracellular Space, Humans, Mice, Inbred C57BL, Mice, Transgenic, Mitochondria, Motor Neurons, Mutation, Spinal Cord, Superoxide Dismutase, Tight Junctions, Endothelial Cells, Microscopy, Electron, Transmission, Mice

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