Wednesday, July 2nd, 2025

Time	Event
4:30p	Transdiagnostic Profiles of BOLD Signal Variability in Autism and Schizophrenia Spectrum Disorders: Associations with Cognition and Functioning Background Autism spectrum disorder (autism) and schizophrenia spectrum disorders (schizophrenia) exhibit overlapping social and neurocognitive impairment and considerable neurobiological heterogeneity. Blood-oxygen-level-dependent (BOLD) signal variability captures the brain's moment-to-moment fluctuations, offering a dynamic marker of neural flexibility that is sensitive to cognitive capacity. This study aimed to examine intra-regional BOLD signal variability during rest and task across schizophrenia, autism, and typically developing controls (TDC) to explore transdiagnostic patterns of brain signal variability and their relationship with cognitive and functional outcomes. Methods Intra-regional BOLD variability, measured by mean squared successive difference (MSSD), was obtained from resting-state and Empathic Accuracy task fMRI in 176 SSD, 89 autism, and 149 TDC participants. ANCOVAs, controlling for age, sex, and motion, assessed group differences in regional and network-level BOLD variability and dimensional associations with social cognition, neurocognition, social functioning, and symptom severity. Results Both autism and schizophrenia exhibited lower BOLD signal variability than TDC across rest and task, with reduced variability observed in somatomotor, visual, and auditory networks (pFDR < 0.01). Greater network variability was positively associated with better social cognitive, neurocognitive, and functional scores across the sample. Resting-state variability showed stronger group-based differences and cognitive associations than task-based variability. Conclusions BOLD signal variability is positively associated with social cognition, neurocognition, and social functioning across groups, suggesting that variability impacts cognitive efficiency and behaviour. Reduced variability in autism and schizophrenia may indicate similar patterns of neural rigidity among these related conditions, positioning BOLD variability as a potential biomarker for neural flexibility and a valuable target for future transdiagnostic clinical interventions. (Comment on this)
4:30p	Sparkling Water Consumption Mitigates Cognitive Fatigue during Prolonged Esports Play Prolonged esports play induces cognitive fatigue, characterized by diminished executive function with pupil constriction. Players often rely on caffeinated or sugary drinks to combat fatigue, but regular use poses health risks. Sparkling water, a sugar- and caffeine-free beverage, stimulates brainstem and prefrontal activity via sensory pathways mediated by transient receptor potential (TRP) channels in the throat. We here tested the hypothesis that sparkling water mitigates cognitive fatigue during prolonged esports play. Fifteen young adult players participated in a randomized crossover trial, each completing two 3-hour sessions of a virtual football game while consuming either sparkling water or plain water. Subjective fatigue, enjoyment, and executive function (via a flanker task) were measured at baseline and hourly, while pupil diameter and heart rate were monitored continuously. Blood glucose and salivary cortisol were also assessed periodically. Compared to plain water, sparkling water significantly attenuated increases in subjective fatigue, enhanced enjoyment, and preserved executive function, along with preventing pupil constriction. Heart rate, blood glucose, and salivary cortisol levels did not differ between conditions. Notably, players committed fewer in-game fouls with sparkling water, while offensive and defensive performance remained unchanged. These findings demonstrate that sparkling water alleviates both subjective and objective signs of cognitive fatigue during prolonged esports play, supporting our hypothesis. This non-caffeinated intervention may help sustain inhibitory control and promote fair behavior, offering a safe and sustainable strategy for managing mental fatigue in modern life. (Comment on this)
4:30p	Neurological Tissue Dissection Techniques in Mouse Models for Reproducible Scientific Results: Brain, Spinal Cord, CSF, and Sciatic Nerve Biomedical research studies, specifically regarding human neurodegenerative diseases, are bound by ethical challenges, and have limited diagnostic and treatment options. Transgenic mouse models offer an incredible research advantage to conduct feasible and practical research with the ability to precisely define the progression of neurodegenerative disease over a well-controlled dosage and timeline. The use of transgenic mouse models has been extensive and is critical to advancing research in many ways, including understanding brain morphology and general tissue changes caused by neurological diseases. Often, these studies require specific brain regions or other neurological tissues which may be difficult to obtain. Unfortunately, specific extraction and dissection protocols are few and far between, leading to inconsistent results and a lack of reproducibility. A well-defined protocol, such as this, is instrumental in overcoming these obstacles and acquiring better experimental results. Five mouse-specific protocols are described: brain extraction, brain microdissection, spinal cord extrusion, cerebral spinal fluid (CSF) collection, and sciatic nerve dissection. Each protocol was completed under biosafety level 2 (BSL-2) guidelines, similar to the sterility precautions required in human surgery. Each protocol also includes a collective materials list that defines proper instruments and usage. The protocol was refined based on feedback from numerous research studies in transcriptomics and pharmaceutical development. These applications require minimizing tissue damage, dissection accuracy, and the ability to reproduce the results, skills that are also directly transferable to clinical settings. The proper implementation of these protocols will allow for more accurate and precise results with reduced variability. This study provides well-defined, succinct, accessible protocols that are more ethical and improve the overall quality of the conducted research. By addressing this need, it supports greater advancements in many cross-disciplinary areas. (Comment on this)
4:30p	Structural Connectome Dimension Shapes Brain Dynamics in Health and Disease The structural connectome serves as the foundation for neural information signaling, playing a primary constraint on brain functionality. Yet, its influence on emergent dynamical properties is not fully understood. Generally, a key measure of a system's structural impact on dynamical phenomena is its dimension. By tracking the temporal evolution of diffusive perturbations, we estimate a scale-dependent measure of dimension of empirical connectomes. At the local scale, it is highly heterogeneous and follows a gradient from sensory-motor to executive areas. At the global scale, it encapsulates mesoscale topological information related to the balance between segregation and integration. Furthermore, by comparing connectomes from stroke patients, we find that dimension captures the local effects of lesions and, at a global level, is linked to impaired critical patterns and decreased cognitive performance. Overall, the dimension of the connectome may serve as a powerful descriptor for bridging the gap between structure and function in the human brain. (Comment on this)
10:15p	Intergenerational Conditioning via Intermittent Parental Hypoxia Confers Stroke Resilience in Offspring Background and Aims: Intergenerational disease transmission, where parental exposures or experiences influence disease susceptibility in offspring, may represent a crucial layer of stroke risk that extends beyond genetics alone. Environmental conditioning, such as intermittent sub-lethal hypoxia, can induce adaptive protective stress responses in the brain. However, whether such parental conditioning enhances offspring resilience to cerebral ischaemia remains unclear. This study investigates whether intermittent hypoxia in parents acts as an intergenerational conditioning stimulus, conferring resilience to ischaemic stroke in offspring, and explores associated molecular mechanisms. Methods: Male and female Balb/C mice (F0) were exposed to intermittent hypoxia (8% O2, 2 hours every other day, 16 cycles) prior to mating. To confirm that intermittent hypoxia induced neuroprotection in the parental generation, a separate cohort of F0 mice underwent transient middle cerebral artery occlusion (tMCAO). Offspring (F1) were generated from hypoxia-exposed F0 breeders and divided into four groups: biparental hypoxia, paternal hypoxia, maternal hypoxia, and normoxic controls. Adult F1 offspring also underwent tMCAO to model ischaemic stroke. Infarct volume and brain swelling were assessed 48 hours post-ischaemia. In a subgroup of F1 offspring, tandem mass tag (TMT)-based proteomic analysis of injured brain tissue was performed post-stroke to identify molecular pathways associated with neuroprotection. Results: Parental intermittent hypoxia significantly reduced infarct size and swelling in F0 mice. These protective effects were inherited by F1 offspring, with biparental exposure producing the greatest reduction in infarct volume, followed by maternal-only and paternal-only groups, and exhibiting sex-specific differences. Proteomic profiling revealed distinct treatment and lineage clusters. Key pathways implicated in offspring neuroprotection included metabolic regulation, immune signalling, cytoskeletal organisation, and cell survival, notably involving PI3K-Akt and EGFR pathways. Conclusions: Intermittent hypoxia in parents acts as an intergenerational conditioning stimulus, conferring offspring resilience to ischaemic stroke. This neuroprotective phenotype is supported by coordinated molecular adaptations in key pathways involved in survival and stress response. These findings highlight the potential for parental environmental conditioning to shape stroke outcomes in offspring, opening new avenues for therapeutic exploration. (Comment on this)
11:35p	Tinnitus perception is linked to arousal system dysfunction Tinnitus, the perception of sound in the absence of an external source, affects 14% of the population and is often associated with concentration and emotional difficulties. However, the characterization of the associated cognitive difficulties remains unclear. We hypothesize that attentional complaints are due to a dysfunction of the exogenous or endogenous orientation of attention, or of the arousal system. In this study, 200 participants (100 with chronic tinnitus and 100 matched controls) completed a battery of cognitive tasks assessing attention, alertness and executive functions, including the Attentional Network Task (ANT), Sustained Attention to Response Task (SART) with mind wandering evaluations, Stroop, and Trail Making Test. Tinnitus comorbidities, including hearing loss, sleep quality, anxiety, and hyperacusis were controlled. The results showed that individuals with tinnitus had a reduced sensitivity to alert signals, and lower sustained attention abilities, both suggesting lower levels of arousal. Mind-wandering analyses revealed fewer planning-related thoughts in the tinnitus group, suggesting higher needed cognitive resources to perform the task. Contrary to prior findings, we found no evidence of deficits in executive functioning specific to tinnitus; rather, executive impairments were associated with hearing loss and sleep disturbances. Overall, these findings support the hypothesis that tinnitus is linked to a dysfunction in the arousal system, likely involving the locus coeruleus, noradrenergic network. This work proposes a new theoretical framework implicating arousal dysregulation as a core mechanism in tinnitus-related cognitive complaints. (Comment on this)

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