Mild Traumatic Brain Injuries and Object Recognition

Qubty, Doaa; Glazer, Sandra; Schreiber, Shaul; Rubovitch, Vardit

doi:10.1016/b978-0-12-812012-5.00022-7

Cited by 3 publications

(2 citation statements)

References 55 publications

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“…Combined with our observation that abnormal neuronal activity developed 7 days after the injury ( Figure 8 ), it is possible that changes in fear conditioning test might result from excess mPFC activity after rmTBI. Our finding of impaired novel object recognition ( Figure 7 ) concurs with others who have used it to show memory deficit and impaired recognition memory after mTBI ( Morawska et al, 2016 ; Qubty et al, 2018 ).…”

Section: Discussionsupporting

confidence: 91%

“…The acute response of brain tissue to a mechanical insult results in ongoing pathology and neurologic outcomes that appear weeks or months following the initial injury (Bramlett and Dietrich, 2015), including diffuse axonal injury (Johnson et al, 2013) and accumulation of amyloid precursor protein (Collins et al, 2020). Furthermore, multiple reports identify mitochondrial dysfunction following mTBI (Vagnozzi et al, 2007;Johnson et al, 2013;Fischer et al, 2016;Kim et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

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Repetitive Mild Traumatic Brain Injury in Rats Impairs Cognition, Enhances Prefrontal Cortex Neuronal Activity, and Reduces Pre-synaptic Mitochondrial Function

Yin

Röth

et al. 2021

Front. Cell. Neurosci.

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A major hurdle preventing effective interventions for patients with mild traumatic brain injury (mTBI) is the lack of known mechanisms for the long-term cognitive impairment that follows mTBI. The closed head impact model of repeated engineered rotational acceleration (rCHIMERA), a non-surgical animal model of repeated mTBI (rmTBI), mimics key features of rmTBI in humans. Using the rCHIMERA in rats, this study was designed to characterize rmTBI-induced behavioral disruption, underlying electrophysiological changes in the medial prefrontal cortex (mPFC), and associated mitochondrial dysfunction. Rats received 6 closed-head impacts over 2 days at 2 Joules of energy. Behavioral testing included automated analysis of behavior in open field and home-cage environments, rotarod test for motor skills, novel object recognition, and fear conditioning. Following rmTBI, rats spent less time grooming and less time in the center of the open field arena. Rats in their home cage had reduced inactivity time 1 week after mTBI and increased exploration time 1 month after injury. Impaired associative fear learning and memory in fear conditioning test, and reduced short-term memory in novel object recognition test were found 4 weeks after rmTBI. Single-unit in vivo recordings showed increased neuronal activity in the mPFC after rmTBI, partially attributable to neuronal disinhibition from reduced inhibitory synaptic transmission, possibly secondary to impaired mitochondrial function. These findings help validate this rat rmTBI model as replicating clinical features, and point to impaired mitochondrial functions after injury as causing imbalanced synaptic transmission and consequent impaired long-term cognitive dysfunction.

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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Repetitive Mild Traumatic Brain Injury in Rats Impairs Cognition, Enhances Prefrontal Cortex Neuronal Activity, and Reduces Pre-synaptic Mitochondrial Function

Yin

Röth

et al. 2021

Front. Cell. Neurosci.

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Photobiomodulation improves functional recovery after mild traumatic brain injury

Stevens,

Hadis,

Thareja

et al. 2024

Bioengineering & Transla Med

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Mild traumatic brain injury (mTBI) is a common consequence of head injury but there are no recognized interventions to promote recovery of the brain. We previously showed that photobiomodulation (PBM) significantly reduced the number of apoptotic cells in adult rat hippocampal organotypic slice cultures. In this study, we first optimized PBM delivery parameters for use in mTBI, conducting cadaveric studies to calibrate 660 and 810 nm lasers for transcutaneous delivery of PBM to the cortical surface. We then used an in vivo weight drop mTBI model in adult rats and delivered daily optimized doses of 660, 810 nm, or combined 660/810 nm PBM. Functional recovery was assessed using novel object recognition (NOR) and beam balance tests, whilst histology and immunohistochemistry were used to assess the mTBI neuropathology. We found that PBM at 810, 660 nm, or 810/660 nm all significantly improved both NOR and beam balance performance, with 810 nm PBM having the greatest effects. Histology demonstrated no overt structural damage in the brain after mTBI, however, immunohistochemistry using brain sections showed significantly reduced activation of both CD11b+ microglia and glial fibrillary acidic protein (GFAP)+ astrocytes at 3 days post‐injury. Significantly reduced cortical localization of the apoptosis marker, cleaved caspase‐3, and modest reductions in extracellular matrix deposition after PBM treatment, limited to choroid plexus and periventricular areas were also observed. Our results demonstrate that 810 nm PBM optimally improved functional outcomes after mTBI, reduced markers associated with apoptosis and astrocyte/microglial activation, and thus may be useful as a potential regenerative therapy.

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A Systematic Review and Meta-Analysis of the Grey Matter Volumetric Changes in Mild Traumatic Brain Injuries

et al. 2022

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Traumatic brain injury (TBI) is currently a problematic issue of public health due to its frequency, and many of the mild cases often remain undiagnosed despite the possible predisposition to prolonged or persistent post-concussive symptomatology. It was shown here that the severity and persistence of grey matter (GM) changes following TBI could predict disease outcomes. Our aim was to conduct a voxel-wise meta-analysis to detect significant GM changes following mild TBI (mTBI) and to investigate whether these changes are associated with the duration and severity of post-concussion syndrome (PCS). A voxel-wise meta-analysis was conducted regarding the GM and white matter (WM) changes in mTBI adult patients versus healthy controls, and Seed-based d Mapping was used to correlate the data. Standard meta-analysis statistical processing was used to assess heterogeneity and publication bias. Our analysis showed significant GM volume increases in the left medial cingulate/paracingulate gyri, the middle frontal gyrus, and the right caudate nucleus of the mTBI patients and significant volume loss in the thalamus, the frontal lobe, and the temporal lobe. These changes could potentially be associated with PCS that some mTBI later patients develop as a result to the injury or other compensatory changes. Additional studies considering long-term GM changes in mTBI patients and their potential relationship to PCS could provide further insight into the pathophysiological similarities and correlations between mTBI and PCS.

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Mild Traumatic Brain Injuries and Object Recognition

Cited by 3 publications

References 55 publications

Repetitive Mild Traumatic Brain Injury in Rats Impairs Cognition, Enhances Prefrontal Cortex Neuronal Activity, and Reduces Pre-synaptic Mitochondrial Function

Repetitive Mild Traumatic Brain Injury in Rats Impairs Cognition, Enhances Prefrontal Cortex Neuronal Activity, and Reduces Pre-synaptic Mitochondrial Function

Photobiomodulation improves functional recovery after mild traumatic brain injury

A Systematic Review and Meta-Analysis of the Grey Matter Volumetric Changes in Mild Traumatic Brain Injuries

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