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The glymphatic system is the macroscopic waste clearance system for the central nervous system. Glymphatic dysfunction has been linked to several neurological conditions, including traumatic brain injury (TBI). Adolescents are at particularly high risk for experiencing a TBI, particularly mild TBI (mTBI) and repetitive mTBI (RmTBI); however, glymphatic clearance, and how it relates to behavioral outcomes, has not been investigated in this context. Therefore, this study examined glymphatic function in the adolescent brain following RmTBI. Female adolescent Sprague Dawley rats were subjected to either three mTBIs or sham injuries spaced three days apart. One-day after their final injury, the animals underwent a beam walking task to assess sensorimotor function, and contrast-enhanced MRI to visualize glymphatic clearance rate. Behavioural measures indicated that the RmTBI group displayed an increase in loss of consciousness as well as motor coordination and balance deficits consistent with our previous studies. The contrast-enhanced MRI results indicated that the female adolescent glymphatic system responds to RmTBI in a region-specific manner, wherein an increased influx but reduced efflux was observed throughout limbic structures (hypothalamus, hippocampus, and amygdala) and the olfactory bulb but neither the influx or efflux were altered in the cortical structures (primary motor cortex, insular cortex, and dorsolateral prefrontal cortex) examined. This may indicate a role for an impaired and/or inefficient glymphatic system in the limbic structures and cortical structures, respectively, in the development of post-concussive symptomology during adolescence.

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In terms of cross-sectional correlations, higher levels of baseline pain intensity and interference were associated with higher levels of baseline PTSS (rs = .35 and .36, ps < .001, respectively), more severe insomnia (r = .22, p < .05 and r = .48, p < .001, respectively), and poorer sleep quality (r = -.20, p < .05 and r = -.40, p < .001, respectively), ps < .05. Higher levels of baseline PTSS were associated with poorer sleep quality (r = -.36, p < .001) and more severe insomnia (r = .49, p < .001). Higher pain interference at follow-up was associated with higher levels of follow-up pain intensity (r = .52, p < .001) and 3-month PTSS (r = .25, p < .05). Longer sleep duration was associated with better sleep quality (r = .20, p < .01). Correlations between objectively assessed sleep duration and most of self-report variables were small and nonsignificant (rs ranged from |.02| to |.16|, ps > .05).With regards to longitudinal correlations, higher levels of pain intensity, pain interference, and PTSS at baseline correlated with higher pain intensity, pain interference, and PTSS at follow-up (rs ranged from .24 to .72, ps < .05). Similarly, more severe insomnia and poorer sleep quality at baseline were associated with higher pain intensity, pain interference, and PTSS at follow-up (rs ranged from |.23| to |.43|, ps < .05). Additional Analyses: Child PTSD Symptom scale (CPSS-5) subscales

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As research regarding the role of circadian rhythms, sleep, and the orexinergic system in neurodegenerative diseases is growing, it is surprising that the choroid plexus (CP) remains underappreciated in this realm. Despite its extensive role in the regulation of circadian rhythms and orexinergic signalling, as well as acting as the primary conduit between cerebrospinal fluid (CSF) and the circulatory system, providing a mechanism by which toxic waste molecules can be removed from the brain, the CP has been largely unexplored in neurodegeneration. In this review, we explore the role of the CP in maintaining brain homeostasis and circadian rhythms, regulating CSF dynamics, and how these functions change across the lifespan, from development to senescence. In addition, we examine the relationship between the CP, orexinergic signalling, and the glymphatic system, highlighting gaps in the literature and areas that require immediate exploration. Finally, we assess current knowledge, including possible therapeutic strategies, regarding the role of the CP in neurological disorders, such as traumatic brain injury, migraine, Alzheimer’s disease, and multiple sclerosis.

An old wives' tale, and strongly held dogma, maintains that one should be kept awake after a mild traumatic brain injury (mTBI) to prevent a coma. This, however, conflicts with the known benefits of sleep: repair and restoration. We therefore sought to examine the effects of sleep deprivation (SD) in the post-traumatic sleep period on post-concussion symptomology (PCS). Adolescent male and female rats were administered repetitive mTBIs (RmTBI) or sham injuries and were then assigned to 5 h of SD or left undisturbed. All animals were then tested using seven behavioral tasks validated to examine PCS, followed by analysis of serum cytokines, and quantitative real-time PCR for messenger RNA (mRNA) expression. Exposure to 3 SD epochs significantly impaired behavior in 4 of 7 of the measures, while RmTBI also produced dysfunction in 5 of 7 tests, but the effects of SD and RmTBI were not cumulative. SD induced long-lasting changes in serum levels of Tnf-α, IL6, and IL-1ß. mRNA expression in the pre-frontal cortex, hippocampus, hypothalamus, and anterior cingulate cortex was modified in response to SD and RmTBI; but similar to the behavioral measures, the mRNA changes were not cumulative. Consequently, we report that SD often produced impairments similar or worse than RmTBI, and sleep hygiene should become a priority for adolescent health.