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Background: Sleep deprivation (SD) is commonplace in modern society and there are large individual differences in the vulnerability to SD. We aim to identify the structural network differences based on diffusion tensor imaging (DTI) that contribute to the individual different vulnerability to SD. Methods: The number of psychomotor vigilance task (PVT) lapses was used to classify 49 healthy subjects on the basis of whether they were vulnerable or resistant to SD. DTI and graph theory approaches were used to investigate the topologic organization differences of the brain structural connectome between SD‐vulnerable and ‐resistant individuals. We measured the level of global efficiency and clustering in rich club and non‐rich club organizations. Results: We demonstrated that participants vulnerable to SD had less global efficiency, network strength, and local efficiency but longer shortest path length compared with participants resistant to SD. Lower efficiency was mainly distributed in the right insula, bilateral thalamus, bilateral frontal, temporal, and temporal lobes. Furthermore, a disrupted subnetwork was observed that consisted of widespread connections. Moreover, the vulnerable group showed significantly decreased strength of the rich club compared with the resistant group. The strength of rich club connectivity was found to be correlated negatively with PVT performance (r = −0.395, p = 0.005). We further tested the reliability of the results. Conclusion: The findings revealed that individual differences in resistance to SD are related to disrupted topologic efficiency connectome pattern, and our study may provide potential connectome‐based biomarkers for the early detection of the vulnerable degree to SD. [ABSTRACT FROM AUTHOR]

Aims: The brain function impairment induced by sleep deprivation (SD) is temporary and can be fully reversed with sufficient sleep. However, in many cases, long‐duration recovery sleep is not feasible. Thus, this study aimed to investigate whether a short nap after SD is sufficient to restore brain function. Methods: The data of 38 subjects, including resting state functional magnetic resonance imaging data collected at three timepoints (before SD, after 30 h of SD, and after a short nap following SD) and psychomotor vigilance task (PVT) data, were collected. Dynamic functional connectivity (DFC) analysis was used to evaluate changes in brain states among three timepoints, and four DFC states were distinguished across the three timepoints. Results: Before SD, state 2 (a resting‐like FC matrix) was dominant (48.26%). However, after 30 h SD, the proportion of state 2 dramatically decreased, and state 3 (still resting‐like, but FCs were weakened) became dominant (40.92%). The increased proportion of state 3 positively correlated with a larger PVT "lapse" time. After a nap, the proportions of states 2 and 3 significantly increased and decreased, respectively, and the change in proportion of state 2 negatively correlated with the change in PVT "lapse" time. Conclusions: Taken together, the results indicated that, after a nap, the cognitive function impairment caused by SD may be reversed to some extent. Additionally, DFC differed among timepoints, which was also associated with the extent of cognitive function impairment after SD (state 3) and the extent of recovery therefrom after a nap (state 2). [ABSTRACT FROM AUTHOR]

Aims In acute stroke, neurological damage is due to oxidative stress and neuronal apoptotic death. This study investigated whether Nogo-A 290-562 residues region (M9), fused to the transduction domain of the HIV trans-activator ( TAT) protein, is neuroprotective against cerebral ischemia and the mechanisms. Methods Transient focal cerebral ischemia was induced by middle cerebral artery occlusion in male C57 BL/6J mice. TAT-M9, its mutation or vehicle was applied via intraperitoneal injection at the onset of reperfusion. The neurobehavioral scores, infarction volumes, neuronal apoptosis, and the ratio of Bax/Bcl-2 were evaluated. Malondialdehyde ( MDA), reactive oxygen species ( ROS) levels, and NADPH oxidase activation were measured in the presence or absence of the NADPH oxidase inhibitor apocynin or activator tetrabromocinnamic acid ( TBCA). Results Immunofluorescence results confirmed that TAT-M9 was transduced into brain parenchyma, and it significantly improved neurological behavior, reduced infarct volumes, protected neuronal cells from apoptosis, inhibited activation of NADPH oxidase, and decreased MDA and ROS contents. Furthermore, apocynin imitated the beneficial effects of TAT-M9, while TBCA abolished them. Conclusions Our results demonstrate that TAT-M9 administration attenuates cerebral ischemia by inhibiting NADPH oxidase-mediated oxidative damage and neuronal apoptosis in mice. TAT-M9 may be a potential treatment for cerebrovascular disease. [ABSTRACT FROM AUTHOR]