Elevating understanding: Linking high-altitude hypoxia to brain aging through EEG functional connectivity and spectral analyses.

High-altitude hypoxia triggers brain function changes reminiscent of those in healthy aging and Alzheimer's disease, compromising cognition and executive functions. Our study sought to validate high-altitude hypoxia as a model for assessing brain activity disruptions akin to aging. We collected EEG data from 16 healthy volunteers during acute high-altitude hypoxia (at 4,000 masl) and at sea level, focusing on relative changes in power and aperiodic slope of the EEG spectrum due to hypoxia. Additionally, we examined functional connectivity using wPLI, and functional segregation and integration using graph theory tools. High altitude led to slower brain oscillations, that is, increased δ and reduced α power, and flattened the 1/f aperiodic slope, indicating higher electrophysiological noise, akin to healthy aging. Notably, functional integration strengthened in the θ band, exhibiting unique topographical patterns at the subnetwork level, including increased frontocentral and reduced occipitoparietal integration. Moreover, we discovered significant correlations between subjects' age, 1/f slope, θ band integration, and observed robust effects of hypoxia after adjusting for age. Our findings shed light on how reduced oxygen levels at high altitudes influence brain activity patterns resembling those in neurodegenerative disorders and aging, making high-altitude hypoxia a promising model for comprehending the brain in health and disease.

Exposure to high-altitude hypoxia, with reduced oxygen levels, can replicate brain function changes akin to aging and Alzheimer's disease. In our work, we propose high-altitude hypoxia as a possible reversible model of human brain aging. We gathered EEG data at high altitude and sea level, investigating the impact of hypoxia on brainwave patterns and connectivity. Our findings revealed that high-altitude exposure led to slower and noisier brain oscillations and produced altered brain connectivity, resembling some remarkable changes seen in the aging process. Intriguingly, these changes were linked to age, even when hypoxia's effects were considered. Our research unveils how high-altitude conditions emulate brain patterns associated with aging and neurodegenerative conditions, providing valuable insights into the understanding of both normal and impaired brain function.

Odor cueing of declarative memories during sleep enhances coordinated spindles and slow oscillations.

Long-term memories are formed by repeated reactivation of newly encoded information during sleep. This process can be enhanced by using memory-associated reminder cues like sounds and odors. While auditory cueing has been researched extensively, few electrophysiological studies have exploited the various benefits of olfactory cueing. We used high-density electroencephalography in an odor-cueing paradigm that was designed to isolate the neural responses specific to the cueing of declarative memories. We show widespread cueing-induced increases in the duration and rate of sleep spindles. Higher spindle rates were most prominent over centro-parietal areas and largely overlapping with a concurrent increase in the amplitude of slow oscillations (SOs). Interestingly, greater SO amplitudes were linked to a higher likelihood of coupling a spindle and coupled spindles expressed during cueing were more numerous in particular around SO up states. We thus identify temporally and spatially coordinated enhancements of sleep spindles and slow oscillations as a candidate mechanism behind cueing-induced memory processing. Our results further demonstrate the feasibility of studying neural activity patterns linked to such processing using olfactory cueing during sleep.

Influence of acute fasting on pain tolerance in healthy subjects: a randomised crossover study.

Background: Although chronic pain and obesity are global health crises with substantial healthcare costs, little is known about the relationship between pain perception and eating behaviours. Food consumption has been reported to provide an analgesic effect by the release of neurotransmitters modulating the pain network. However, whether short-term (acute) fasting affects pain perception remains unclear. Purpose: This study aimed to investigate the effect of acute fasting on pain perception and whether attention and mood changes drove the observed changes. Patients and methods: The cold pressor test (CPT) was used to investigate the pain tolerance of 25 healthy participants in both non-fasting and 12-h fasting sessions. They were randomised to either session with a crossover to the other after at least 24 h, with the experimenter blinded to the sessions. The pain tolerance was measured using a Stroop task in both attentive and distracted states. The Profile of Mood States (POMS) questionnaire was used to capture the mood, and a 10-point hunger scale was used to measure hunger. Mixed-effects models were used to investigate the influence of fasting and distraction on pain perception, accounting for the repeated measures. Results: Fasting reduced CPT pain tolerance, with fasting participants twice as likely to withdraw their hands early (hazard ratio = 2.4, 95% CI: 1.3-4.5). Though men tolerated CPT pain longer than women, there was no evidence that men responded to fasting differently than women (p = 0.9). In addition, no evidence supporting that fasting affected attention or mood was found. Nonetheless, it increased hunger scores by 2.7 points on a 10-point scale (95% CI: 1.2-4.2) and decreased blood glucose concentration levels by 0.51 mmol/L (95% CI: 0.19-0.84). Conclusion: Acute fasting reduces pain tolerance in the healthy participants, and this effect is independent of gender and attention or mood changes.

DIVA Meets EEG: Model Validation Using Formant-Shift Reflex.

The neurocomputational model 'Directions into Velocities of Articulators' (DIVA) was developed to account for various aspects of normal and disordered speech production and acquisition. The neural substrates of DIVA were established through functional magnetic resonance imaging (fMRI), providing physiological validation of the model. This study introduces DIVA_EEG an extension of DIVA that utilizes electroencephalography (EEG) to leverage the high temporal resolution and broad availability of EEG over fMRI. For the development of DIVA_EEG, EEG-like signals were derived from original equations describing the activity of the different DIVA maps. Synthetic EEG associated with the utterance of syllables was generated when both unperturbed and perturbed auditory feedback (first formant perturbations) were simulated. The cortical activation maps derived from synthetic EEG closely resembled those of the original DIVA model. To validate DIVA_EEG, the EEG of individuals with typical voices (N = 30) was acquired during an altered auditory feedback paradigm. The resulting empirical brain activity maps significantly overlapped with those predicted by DIVA_EEG. In conjunction with other recent model extensions, DIVA_EEG lays the foundations for constructing a complete neurocomputational framework to tackle vocal and speech disorders, which can guide model-driven personalized interventions.

Altered Pain Processing Associated with Administration of Dopamine Agonist and Antagonist in Healthy Volunteers.

Striatal dopamine dysfunction is associated with the altered top-down modulation of pain processing. The dopamine D2-like receptor family is a potential substrate for such effects due to its primary expression in the striatum, but evidence for this is currently lacking. Here, we investigated the effect of pharmacologically manipulating striatal dopamine D2 receptor activity on the anticipation and perception of acute pain stimuli in humans. Participants received visual cues that induced either certain or uncertain anticipation of two pain intensity levels delivered via a CO2 laser. Rating of the pain intensity and unpleasantness was recorded. Brain activity was recorded with EEG and analysed via source localisation to investigate neural activity during the anticipation and receipt of pain. Participants completed the experiment under three conditions, control (Sodium Chloride), D2 receptor agonist (Cabergoline), and D2 receptor antagonist (Amisulpride), in a repeated-measures, triple-crossover, double-blind study. The antagonist reduced an individuals' ability to distinguish between low and high pain following uncertain anticipation. The EEG source localisation showed that the agonist and antagonist reduced neural activations in specific brain regions associated with the sensory integration of salient stimuli during the anticipation and receipt of pain. During anticipation, the agonist reduced activity in the right mid-temporal region and the right angular gyrus, whilst the antagonist reduced activity within the right postcentral, right mid-temporal, and right inferior parietal regions. In comparison to control, the antagonist reduced activity within the insula during the receipt of pain, a key structure involved in the integration of the sensory and affective aspects of pain. Pain sensitivity and unpleasantness were not changed by D2R modulation. Our results support the notion that D2 receptor neurotransmission has a role in the top-down modulation of pain.

An unsuccessful attempt to demonstrate attentional orienting within the purely emotional domain.

Inhibition of return (IOR) is an attentional effect that has been much researched in the spatial domain, whereby people are slower to respond to stimuli presented in a previously attended location. Recently, Chao (2010) reported that participants were slower to respond to a negative schematic facial target compared with a positive facial target if they had previously viewed a cue with a negative expression, which he interpreted as IOR in the purely emotional domain. That is, once their attention is drawn away, people are slower to reattend to negative emotions. Here, we investigated whether this effect could be observed when controlling for the valence of the target and when using a more naturalistic human facial expression as a cue. We replicated Chao's findings using real face cues, observing slower responses for negative cues followed by negative versus positive targets, and faster responses for positive cues followed by positive versus negative targets. However, our reanalysis indicates that these effects are better accounted for by the valence (positive/negative) of the target, with responses being slower to negative compared with positive facial expressions regardless of the preceding cue. In conclusion, orienting in the emotional domain could not be measured using a cue-target task, as the effect of responding to emotional targets eclipsed any potential emotional cuing effect.