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Overlapping symptoms between Alzheimers disease (AD), behavioral variant of frontotemporal dementia (bvFTD), and schizophrenia (SZ) can lead to misdiagnosis and delays in appropriate treatment, especially in cases of early-onset dementia. To determine the potential of brain signal variability as a diagnostic tool, we assessed the coefficient of variation of the BOLD signal (CVBOLD) in 234 participants spanning bvFTD (n = 53), AD (n = 17), SZ (n = 23), and controls (n = 141). All underwent functional and structural MRI scans. Data unveiled a notable increase in CVBOLD in bvFTD patients across both datasets (local and international, p

Introduction: The cerebrospinal fluid dynamics in the human brain are driven by physiological pulsations, including cardiovascular pulses and very low-frequency (< 0.1Hz) vasomotor waves. Ultrafast functional magnetic resonance imaging (fMRI) facilitates the simultaneous measurement of these signals from venous and arterial compartments independently with both classical venous blood oxygenation level dependent (BOLD) and faster arterial spin-phase contrast. Methods: In this study, we compared the interaction of these two pulsations in awake and sleep using fMRI and peripheral fingertip photoplethysmography in both arterial and venous signals in 10 healthy subjects (5 female). Results: Sleep increased the power of brain cardiovascular pulsations, decreased peripheral pulsation, and desynchronized them. However, vasomotor waves increase power and synchronicity in both brain and peripheral signals during sleep. Peculiarly, lag between brain and peripheral vasomotor signals reversed in sleep within the default mode network. Finally, sleep synchronized cerebral arterial vasomotor waves with venous BOLD waves within distinct parasagittal brain tissue. Discussion: These changes in power and pulsation synchrony may reflect systemic sleep-related changes in vascular control between the periphery and brain vasculature, while the increased synchrony of arterial and venous compartments may reflect increased convection of regional neurofluids in parasagittal areas in sleep. [ABSTRACT FROM AUTHOR]

Previous studies have suggested that atypical deactivation of functional brain networks contributes to the complex cognitive and behavioral profile associated with autism spectrum disorder (ASD). However, these studies have not considered the temporal dynamics of deactivation mechanisms between the networks. In this study, we examined (a) mutual deactivation and (b) mutual activation‐deactivation (i.e., anticorrelated) time‐lag patterns between resting‐state networks (RSNs) in young adults with ASD (n = 20) and controls (n = 20) by applying the recently defined dynamic lag analysis (DLA) method, which measures time‐lag variations peak‐by‐peak between the networks. In order to achieve temporally accurate lag patterns, the brain imaging data was acquired with a fast functional magnetic resonance imaging (fMRI) sequence (TR = 100 ms). Group‐level independent component analysis was used to identify 16 RSNs for the DLA. We found altered mutual deactivation timings in ASD in (a) three of the deactivated and (b) two of the transiently anticorrelated (activated‐deactivated) RSN pairs, which survived the strict threshold for significance of surrogate data. Of the significant RSN pairs, 80% included the posterior default‐mode network (DMN). We propose that temporally altered deactivation mechanisms, including timings and directionality, between the posterior DMN and RSNs mediating processing of socially relevant information may contribute to the ASD phenotype. Lay Summary To understand autistic traits on a neural level, we examined temporal fluctuations in information flow between brain regions in young adults with autism spectrum disorder (ASD) and controls. We used a fast neuroimaging procedure to investigate deactivation mechanisms between brain regions. We found that timings and directionality of communication between certain brain regions were temporally altered in ASD, suggesting atypical deactivation mechanisms associated with the posterior default‐mode network. [ABSTRACT FROM AUTHOR]

Introduction: Sleep increases brain fluid transport and the power of pulsations driving the fluids. We investigated how sleep deprivation or electrophysiologically different stages of non-rapid-eye-movement (NREM) sleep affect the human brain pulsations., Methods: Fast functional magnetic resonance imaging (fMRI) was performed in healthy subjects ( n  = 23) with synchronous electroencephalography (EEG), that was used to verify arousal states (awake, N1 and N2 sleep). Cardiorespiratory rates were verified with physiological monitoring. Spectral power analysis assessed the strength, and spectral entropy assessed the stability of the pulsations., Results: In N1 sleep, the power of vasomotor (VLF < 0.1 Hz), but not cardiorespiratory pulsations, intensified after sleep deprived vs. non-sleep deprived subjects. The power of all three pulsations increased as a function of arousal state (N2 > N1 > awake) encompassing brain tissue in both sleep stages, but extra-axial CSF spaces only in N2 sleep. Spectral entropy of full band and respiratory pulsations decreased most in N2 sleep stage, while cardiac spectral entropy increased in ventricles., Discussion: In summary, the sleep deprivation and sleep depth, both increase the power and harmonize the spectral content of human brain pulsations., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The author(s) declared that they were an editorial board member of Frontiers, at the time of submission. This had no impact on the peer review process and the final decision., (Copyright © 2023 Helakari, Järvelä, Väyrynen, Tuunanen, Piispala, Kallio, Ebrahimi, Poltojainen, Kananen, Elabasy, Huotari, Raitamaa, Tuovinen, Korhonen, Nedergaard and Kiviniemi.)

Previous studies have suggested that atypical deactivation of functional brain networks contributes to the complex cognitive and behavioral profile associated with autism spectrum disorder (ASD). However, these studies have not considered the temporal dynamics of deactivation mechanisms between the networks. In this study, we examined (a) mutual deactivation and (b) mutual activation-deactivation (i.e., anticorrelated) time-lag patterns between resting-state networks (RSNs) in young adults with ASD (n = 20) and controls (n = 20) by applying the recently defined dynamic lag analysis (DLA) method, which measures time-lag variations peak-by-peak between the networks. In order to achieve temporally accurate lag patterns, the brain imaging data was acquired with a fast functional magnetic resonance imaging (fMRI) sequence (TR = 100 ms). Group-level independent component analysis was used to identify 16 RSNs for the DLA. We found altered mutual deactivation timings in ASD in (a) three of the deactivated and (b) two of the transiently anticorrelated (activated-deactivated) RSN pairs, which survived the strict threshold for significance of surrogate data. Of the significant RSN pairs, 80% included the posterior default-mode network (DMN). We propose that temporally altered deactivation mechanisms, including timings and directionality, between the posterior DMN and RSNs mediating processing of socially relevant information may contribute to the ASD phenotype. LAY SUMMARY: To understand autistic traits on a neural level, we examined temporal fluctuations in information flow between brain regions in young adults with autism spectrum disorder (ASD) and controls. We used a fast neuroimaging procedure to investigate deactivation mechanisms between brain regions. We found that timings and directionality of communication between certain brain regions were temporally altered in ASD, suggesting atypical deactivation mechanisms associated with the posterior default-mode network., (© 2020 International Society for Autism Research and Wiley Periodicals LLC.)