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To determine if creatine (Cr) supplementation could influence cognitive performance and whether any changes were related to changes in prefrontal cortex (PFC) activation during such cognitive tasks, thirty (M = 11, F = 19) participants were evenly randomized to receive supplementation with Cr (CR10:10 g/day or CR20:20 g/day) or a placebo (PLA:10 g/day) for 6 weeks. Participants completed a cognitive test battery (processing speed, episodic memory, and attention) on two separate occasions prior to and following supplementation. Functional near-infrared spectroscopy (fNIRS) was used to measure PFC oxyhemoglobin (O2Hb) during the cognitive evaluation. A two-way repeated measures ANOVA was used to determine the differences between the groups and the timepoints for the cognitive performance scores and PFC O2Hb. In addition, a one-way ANOVA of % change was used to determine pre- and post-differences between the groups. Creatine (independent of dosage) had no significant effect on the measures of cognitive performance. There was a trend for decreased relative PFC O2Hb in the CR10 group versus the PLA group in the processing speed test (p = 0.06). Overall, six weeks of Cr supplementation at a moderate or high dose does not improve cognitive performance or change PFC activation in young adults.

(1) Background: Cerebral autoregulation is altered during acute mild traumatic brain injury, or concussion. However, it is unknown how a history of concussion can impact cerebral haemodynamic activity during a task that elicits an autoregulatory response. (2) Methods: We assessed cerebral haemodynamic activity in those with a history of three or more concussions. The study included 44 retired athletes with concussion history and 25 control participants. We recorded participants’ relative changes in right and left pre-frontal cortex oxygenation collected by near-infrared spectroscopy and continuous beat-to-beat blood pressure measured by finger photoplethysmography. Participants completed a 5-min seated rest followed by a 5-min repeated squat (10-s) stand (10-s) maneuver (0.05 Hz) to elicit a cerebral autoregulatory response. Wavelet transformation was applied to the collected signals, allowing separation into cardiac interval I (0.6 to 2 Hz), respiratory interval II (0.145 to 0.6 Hz), and smooth muscle cell interval III (0.052 to 0.145 Hz). (3) Results: Significant increases at cardiac interval I were found for the wavelet amplitude of oxy-haemoglobin and haemoglobin difference at the right pre-frontal cortex. No significant difference was found at the left pre-frontal cortex or the blood pressure wavelet amplitudes. (4) Conclusions: Contributions from cardiac activity to the pre-frontal cortex oxygenation are elevated when eliciting dynamic cerebral autoregulation in those with a history of three or more concussions.

Sleep deprivation leads to the deterioration in the physiological functioning of the brain, cognitive decline, and many neurodegenerative diseases, all of which progress with advancing age. Sleep insufficiency and impairments in cognitive function are characterized by progressive neuronal losses in the cerebral cortex. In this study, we analyze gene expression profiles following sleep-deprived murine models and circadian matched controls to identify genes that might underlie cortical homeostasis in response to sleep deprivation. Screening of the literature resulted in three murine (Mus musculus) gene expression datasets (GSE6514, GSE78215, and GSE33491) that included cortical tissue biopsies from mice that are sleep deprived for 6 h (n = 15) and from circadian controls that are left undisturbed (n = 15). Cortical differentially expressed genes are used to construct a network of encoded proteins that are ranked based on their interactome according to 11 topological algorithms. The analysis revealed three genes—NFKBIA, EZR, and SGK1—which exhibited the highest multi-algorithmic topological significance. These genes are strong markers of increased brain inflammation, cytoskeletal aberrations, and glucocorticoid resistance, changes that imply aging-like transcriptional responses during sleep deprivation in the murine cortex. Their potential role as candidate markers of local homeostatic response to sleep loss in the murine cortex warrants further experimental validation.