Mild Traumatic Brain Injury Contributes to the Development of Delayed Neuroinflammation

Abstract

<b><i>Introduction:</i></b> In recent years, according to the literature, the problem of mild traumatic brain injury (mTBI) has become more and more urgent. Compared to moderate to severe craniocerebral trauma, mTBI occurs in a far greater number of people. The delayed sequelae caused by a single mTBI or multiple mTBIs are a significant public health problem. <b><i>Methods:</i></b> A weight-drop model was used for the formation of mTBI. A metal rod weighing 337 g with a blunt tip of 3 mm diameter was uplifted at 8 cm height and held by a lever. The trauma was created by lowering the lever and the rod and free-dropping onto the rat skull. In the cerebral cortex of experimental animals, we analyzed the level of microglial activity (Iba-1-positive system) and the expression of pro-inflammatory markers (IL1β, IL6, and CD86). Also, the expression level of the endocannabinoid system receptor (cannabinoid receptor type 1 [CB1]) was assessed in brain samples. <b><i>Results:</i></b> Experiments have shown that mTBI increases (1) the amount of microglia (iba-1) activated by the pro-inflammatory pathway (CD86); (2) the level of pro-inflammatory cytokines IL1β and IL6; and (3) CB1R activity. <b><i>Conclusion:</i></b> Overall, the results of this study indicate that mTBI induces a sustained neuroinflammatory response.

Amyloid PET across the cognitive spectrum in former professional and college American football players: findings from the DIAGNOSE CTE Research Project

“…That is, is there a potential mechanism that would reduce or prevent Aβ neuritic plaques in individuals with extensive RHI exposure? Animal models have shown that there is microglial activation with a sustained inflammatory response during and following repetitive mTBI [ 50 – 53 ], but before p-tau pathology [ 54 ]. In a postmortem study of young contact sport athletes, an increased number of activated microglia, positively associated with CTE severity, has been reported [ 55 ].…”

Sex-specific differences in rotarod performance and type 1 cannabinoid receptor levels in a rat model of traumatic brain injury treated with Δ9-tetrahydrocannabinol

“…Several studies have explored the ECS and effects of cannabinoids on TBI in rodent models with several recent studies reporting elevated CB1R activity (Xing et al, 2014;Arain et al, 2015;Ponomarenko et al, 2021). In particular, one study by Bhatt et.…”

Synaptamide Modulates Astroglial Activity in Mild Traumatic Brain Injury

“…Astrocyte-driven neuroinflammation is maintained by other cell populations, such as microglia/macrophages, as well as lymphocytes recruited from the peripheral blood. Our previous studies demonstrate an increase in the inflammatory activity of microglia and the synthesis of pro-inflammatory cytokines only on the 7th day after surgery [ 14 ], while on the first day microgliosis is not so pronounced [ 33 ]. In the delayed period of TBI, astrocytes perform a rather neuroprotective function by secreting neurotrophins and participating in synapse remodeling through the production of extracellular matrix molecules [ 34 ].…”