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Acute Traumatic Brain Injury Does Not Exacerbate Amyotrophic Lateral Sclerosis in the SOD1 G93A Rat Model

Thomsen, Gretchen M., Vit, Jean-Philippe, Lamb, Alexander, Gowing, Genevieve, Shelest, Oksana, Alkaslasi, Mor, Ley, Eric J., Svendsen, Clive N.·2015·eneuro
DOI 10.1523/eneuro.0059-14.2015PMC PMC4586929
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Abstract

Amyotrophic lateral sclerosis (ALS) is a fatal motor neuron disease in which upper and lower motor neurons degenerate, leading to muscle atrophy, paralysis, and death within 3 to 5 years of onset. While a small percentage of ALS cases are genetically linked, the majority are sporadic with unknown origin. Currently, etiological links are associated with disease onset without mechanistic understanding. Of all the putative risk factors, however, head trauma has emerged as a consistent candidate for initiating the molecular cascades of ALS. Here, we test the hypothesis that traumatic brain injury (TBI) in the SOD1 G93A transgenic rat model of ALS leads to early disease onset and shortened lifespan. We demonstrate, however, that a one-time acute focal injury caused by controlled cortical impact does not affect disease onset or survival. Establishing the negligible involvement of a single acute focal brain injury in an ALS rat model increases the current understanding of the disease. Critically, untangling a single focal TBI from multiple mild injuries provides a rationale for scientists and physicians to increase focus on repeat injuries to hopefully pinpoint a contributing cause of ALS.

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Crossref · 10.1523/eneuro.0059-14.2015

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Figure 1 A, Coronal brain sections (420 µm apart, notched on the ipsilateral underside prior to sectioning) stained with cresyl violet from a rat that was administered a moderate CCI at P120. B, Quantitative analysis of the cortical lesion site after TBI revealed that this moderate CCI injury resulted in an ∼30% loss of tissue in both WT and SOD1 rats [30.5 ± 3.7% (SEM) in WT and 30.4 ± 1.1% in SOD1 rats, ipsilateral tissue loss, relative to the contralateral cortex]. C–F, This injury did not result in overt functional deficits in either WT or SOD1 rats, relative to their sham counterparts, during the early time points after injury (time points P126–P153) as assessed by (C) hindlimb and (D) forelimb grip strength, as well as (E) hindlimb and (F) forelimb BBB scores. C–H, Injured SOD1 rats showed no differences in strength or motor function relative to SOD1 sham rats at later time points (C–F) and there was no effect of TBI on (G) disease onset or (H) survival, supporting the idea that a one-time acute moderate TBI in rats close to disease onset does not predispose earlier onset or death. P.I.D. 1: post-injury day 1; Scale bar, 2 mm.
Figure 1 A, Coronal brain sections (420 µm apart, notched on the ipsilateral underside prior to sectioning) stained with cresyl violet from a rat that was administered a moderate CCI at P120. B, Quantitative analysis of the cortical lesion site after TBI revealed that this moderate CCI injury resulted in an ∼30% loss of tissue in both WT and SOD1 rats [30.5 ± 3.7% (SEM) in WT and 30.4 ± 1.1% in SOD1 rats, ipsilateral tissue loss, relative to the contralateral cortex]. C–F, This injury did not result in overt functional deficits in either WT or SOD1 rats, relative to their sham counterparts, during the early time points after injury (time points P126–P153) as assessed by (C) hindlimb and (D) forelimb grip strength, as well as (E) hindlimb and (F) forelimb BBB scores. C–H, Injured SOD1 rats showed no differences in strength or motor function relative to SOD1 sham rats at later time points (C–F) and there was no effect of TBI on (G) disease onset or (H) survival, supporting the idea that a one-time acute moderate TBI in rats close to disease onset does not predispose earlier onset or death. P.I.D. 1: post-injury day 1; Scale bar, 2 mm.CC BY · PubMed Central
Figure 2 A, Coronal brain sections (420 µm apart, notched on the contralateral underside prior to sectioning) stained with cresyl violet from a rat administered a severe CCI at P90. B, Quantitative analysis of the cortical lesion site after TBI revealed that this severe CCI injury resulted in an ∼45% loss of tissue in both WT and SOD1 rats [44.3 ± 3.3% (SEM) in WT and 48.4 ± 3.5% in SOD1, ipsilateral tissue volume loss, relative to the contralateral cortex]. C, This severe CCI injury resulted in significant early postinjury deficits (graph time points P91–P97) in both WT and SOD1 injured rats, relative to their sham counterparts in rotarod performance. D, E, Relative to SOD1 sham rats, injured SOD1 rats showed a significant overall decrease due to injury in (D) hindlimb, but not (E) forelimb, grip strength. F–I, However, measures of disease such as (F) onset, (G) survival, and (H) hindlimb and (I) forelimb BBB scores remained unchanged relative to SOD1 sham controls, indicating that a one-time severe acute TBI at an early presymptomatic time point does not affect the disease onset or death in these rats. P.I.D. 1: post-injury day 1; Scale bar, 2 mm.
Figure 2 A, Coronal brain sections (420 µm apart, notched on the contralateral underside prior to sectioning) stained with cresyl violet from a rat administered a severe CCI at P90. B, Quantitative analysis of the cortical lesion site after TBI revealed that this severe CCI injury resulted in an ∼45% loss of tissue in both WT and SOD1 rats [44.3 ± 3.3% (SEM) in WT and 48.4 ± 3.5% in SOD1, ipsilateral tissue volume loss, relative to the contralateral cortex]. C, This severe CCI injury resulted in significant early postinjury deficits (graph time points P91–P97) in both WT and SOD1 injured rats, relative to their sham counterparts in rotarod performance. D, E, Relative to SOD1 sham rats, injured SOD1 rats showed a significant overall decrease due to injury in (D) hindlimb, but not (E) forelimb, grip strength. F–I, However, measures of disease such as (F) onset, (G) survival, and (H) hindlimb and (I) forelimb BBB scores remained unchanged relative to SOD1 sham controls, indicating that a one-time severe acute TBI at an early presymptomatic time point does not affect the disease onset or death in these rats. P.I.D. 1: post-injury day 1; Scale bar, 2 mm.CC BY · PubMed Central

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Metadata

Authors
Thomsen, G. M., Vit, J.-P., Lamb, A., Gowing, G., Shelest, O., Alkaslasi, M., Ley, E. J., & Svendsen, C. N.
ORCID
Venue
eneuro
Publisher
Society for Neuroscience
Published
2015-05
Volume
2
Issue
3
Pages
ENEURO.0059-14.2015
ISSN
2373-2822
DOI
10.1523/eneuro.0059-14.2015
PMC
PMC4586929
Cited by
13
References
5
Language
en
Funders
  • ALS Association
  • Board of Governors Regenerative Medicine Institute

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Thomsen, G. M., Vit, J.-P., Lamb, A., Gowing, G., Shelest, O., Alkaslasi, M., Ley, E. J., & Svendsen, C. N. (2015). Acute Traumatic Brain Injury Does Not Exacerbate Amyotrophic Lateral Sclerosis in the SOD1 G93A Rat Model. eneuro. https://doi.org/10.1523/eneuro.0059-14.2015