Abstract
Little is known about the impairments and pathological changes in the visual system in mild brain trauma, especially repetitive mild traumatic brain injury (mTBI). The goal of this study was to examine and compare the effects of repeated head impacts on the neurodegeneration, axonal integrity, and glial activity in the optic tract (OT), as well as on neuronal preservation, glial responses, and synaptic organization in the lateral geniculate nucleus (LGN) and superior colliculus (SC), in wild-type mice and transgenic animals with overexpression of human TDP-43 mutant protein (TDP-43G348C) at 6 months after repeated closed head traumas. Animals were also assessed in the Barnes maze (BM) task. Neurodegeneration, axonal injury, and gliosis were detected in the OT of the injured animals of both genotypes. In the traumatized mice, myelination of surviving axons was mostly preserved, and the expression of neurofilament light chain was unaffected. Repetitive mTBI did not induce changes in the LGN and the SC, nor did it affect the performance of the BM task in the traumatized wild-type and TDP-43 transgenic mice. Differences in neuropathological and behavioral assessments between the injured wild-type and TDP-43G348C mice were not revealed. Results of the current study suggest that repetitive mTBI was associated with chronic damage and inflammation in the OT in wild-type and TDP-43G348C mice, which were not accompanied with behavioral problems and were not affected by the TDP-43 genotype, while the LGN and the SC remained preserved in the used experimental conditions.
Highlights
Repetitive mild traumatic brain injury represents a current and growing serious medical and economic problem worldwide
Repetitive mild traumatic brain injury (mTBI) has long been recognized as a risk factor for chronic traumatic encephalopathy (CTE), a condition characterized by generalized cerebral atrophy associated with widespread deposits of phosphorylated tau protein occurring as neurofibrillary tangles, diffuse beta-amyloid deposits, neuroinflammation, axonal pathology through the brain, and, in the majority of cases, by transactivation response element (TAR) DNA/RNA-binding protein 43 (TDP-43) immunoreactive intraneuronal and intraglial inclusions [10,11,12,13]
Equal neurofilament light (NfL)-positive staining was revealed in the axons of the optic tract (OT) in the traumatized and the sham mice of both genotypes (Figure 4A), while a significant difference in the NfL optical densities between the experimental groups was not revealed (p = 0.254) (Figure 4B). These results suggest that the NfL expression in the axons of the OT was unchanged at 6 months following repetitive mTBI
Summary
Repetitive mild traumatic brain injury (mTBI) represents a current and growing serious medical and economic problem worldwide. It is common in athletes engaged in contact sports, such as soccer, ice hockey, American football, boxing, wrestling, and mixed martial arts [1,2], as well as in victims of domestic spousal violence or child abuse [3] and military personnel [4,5]. Repetitive mTBI has long been recognized as a risk factor for chronic traumatic encephalopathy (CTE), a condition characterized by generalized cerebral atrophy associated with widespread deposits of phosphorylated tau protein occurring as neurofibrillary tangles, diffuse beta-amyloid deposits, neuroinflammation, axonal pathology through the brain, and, in the majority of cases, by transactivation response element (TAR) DNA/RNA-binding protein 43 (TDP-43) immunoreactive intraneuronal and intraglial inclusions [10,11,12,13]
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