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T 2 -Weighted MRI Detects Presymptomatic Pathology in the SOD1 Mouse Model of ALS
Open accessAbstract
Neuroinflammation has been identified as a potential therapeutic target in amyotrophic lateral sclerosis (ALS), but relevant biomarkers are needed. The superoxide dismutase (SOD1) G93A transgenic mouse model of ALS offers a unique opportunity to study and potentially manipulate presymptomatic pathology. While T 2 -weighted magnetic resonance imaging (MRI) has been shown to be sensitive to pathologic changes at symptom onset, no earlier biomarkers were previously identified and the underlying histopathologic correlates remain uncertain. To address these issues, we used a multimodal MRI approach targeting structural ( T 2 , T 2 , apparent diffusion coefficient (ADC), magnetization transfer ratio (MTR)), vascular (gadolinium diethylene triamine pentaacetic acid), and endothelial (vascular cell adhesion molecule-microparticles of iron oxide) changes, together with histopathologic analysis from presymptomatic to symptomatic stages of disease. Presymptomatic changes in brainstem nuclei were evident on T 2 -weighted images from as early as 60 days ( P<0.05). Histologic indices of vacuolation, astro- and microglial activation all correlated with T 2 -weighted changes. Significant reductions in ADC ( P<0.01) and MTR ( P<0.05) were found at 120 days in the same brainstem nuclei. No changes in T 1 relaxation, vascular permeability, or endothelial activation were found at any stage of disease. These findings suggest that T 2 -weighted MRI offers the strongest biomarker potential in this model, and that MRI has unique potential for noninvasive and longitudinal assessment of presymptomatically applied therapeutic and neuroprotective agents.
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One study failed to detect any T1-enhancement after gadolinium injection in SOD1 G93A mice, suggesting no change in BBB and BSCB integrity.
“One study, however, failed to detect any T1-enhancement after gadolinium injection in SOD1 G93A mice, suggesting no change in BBB and BSCB integrity (166), in contrast to several independent previous studies discussed above showing disrupted BSCB and BBB in SOD1 G93A mice (20, 50, 51, 194, 196, 415, 431, 432, 687, 688).”
From Blood-Brain Barrier: From Physiology to Disease and Back (2019) · cites this paper as [166]
The Results section (page unavailable) reports no increase in brain vascular permeability on gadolinium-enhanced T1 MRI in SOD1G93A mice. The Figure 5 caption also says no change was seen in the spinal cord, but the paper does not clearly report a spinal-cord T1-enhancement result. Thus the BBB finding is supported, while the claim that the gadolinium result establishes unchanged BSCB integrity goes beyond the stated evidence. (LLM, conf=0.84)
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Self-citationALS-causing SOD1 mutants generate vascular changes prior to motor neuron degeneration
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Blood-Brain Barrier: From Physiology to Disease and Back
Sweeney, M. D., Zhao, Z., Montagne, A., Nelson, A. R., & Zlokovic, B. V. (2019) · Physiological Reviews · doi:10.1152/physrev.00050.2017 · Cited by 2,312
Mouse models of neurodegenerative disease: preclinical imaging and neurovascular component
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Metadata
- Authors
- Evans, M. C., Serres, S., Khrapitchev, A. A., Stolp, H. B., Anthony, D. C., Talbot, K., Turner, M. R., & Sibson, N. R.
- Affiliations
- University of Oxford (GB)
- Corresponding author
- Turner, Martin R
- ORCID
- Venue
- Journal of Cerebral Blood Flow & Metabolism
- Publisher
- SAGE Publications
- Published
- 2014-02-05
- Volume
- 34
- Issue
- 5
- Pages
- 785-793
- ISSN
- 0271-678X (ISSN-L)
- 1559-7016
- PMC
- PMC4013759
- OpenAlex
- W2030984455
- Cited by
- 37
- References
- 3
- Citations by year
- 2025: 2 · 2024: 2 · 2023: 1 · 2022: 3 · 2021: 1 · 2020: 6 · 2019: 1 · 2018: 8 · 2017: 6 · 2016: 2 · 2015: 2 · 2014: 3
- FWCI
- 2.83
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- Journal of Cerebral Blood Flow & Metabolism (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Research Portal (King's College London) (publishedVersion, other-oa)
- Repository@Nottingham (University of Nottingham) (publishedVersion, cc-by)
- Repository@Nottingham (University of Nottingham) (submittedVersion, cc-by)
- RVC Research Online (Royal Veterinary College) (submittedVersion, cc-by)
- Funders
- Cancer Research UK (C5255, A12678, 16945, C5255/A12678)
- Motor Neurone Disease Association (G0701923, TURNER/JAN13/944-795)
- Medical Research Council (C5255/A12678, G0701923)
- Topics
- Health Sciences › Medicine › Clinical Neurology › Amyotrophic Lateral Sclerosis Research
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Advanced MRI Techniques and Applications
- Health Sciences › Medicine › Clinical Neurology › Multiple Sclerosis Research Studies
- Keywords
- amyotrophic lateral sclerosis, T2-weighted MRI, neuroinflammation, brainstem nuclei, apparent diffusion coefficient, magnetization transfer ratio, Gd-DTPA, iron oxide microparticles, astrocyte activation, microglial activation, vacuolization, MRI biomarkers, neuroprotection
- MeSH terms
- Superoxide Dismutase-1, Amyotrophic Lateral Sclerosis, Animals, Astrocytes, Blood-Brain Barrier, Brain Stem, Disease Models, Animal, Humans, Magnetic Resonance Imaging, Mice, Transgenic, Motor Activity, Mutation, Permeability, Spinal Cord, Superoxide Dismutase, Weight Loss, Microglia, Mice
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