26.04.2026, Sunday, 10:30-12:00
General focus of the symposium:
This symposium aims to bring together complementary lines of research that examine how the human brain responds to strain, whether triggered acutely by physiological conditions and cognitive demands, or chronically by affective disorders. Evidence will be provided on how neural systems adjust under such pressures, revealing functional dynamics and structural changes that support, or compromise, adaptive functioning and mental health. One example of acute physiological strain comes from research on cold-water immersion (CWI). Although CWI is increasingly recognised for improving mood and decreasing depressive symptoms, less is known about the underlying processes that accompany these behavioural effects. Drawing on resting-state functional magnetic resonance imaging (fMRI) data, recent findings show that brief CWI prompts specific adjustments in large-scale network organisation. This offers new insight into how the brain responds to immediate physiological challenge and how these adaptations facilitate mood improvements. Cognitive strain offers another example of how the brain responds to immediate challenge. Tasks involving conflict or unpredictability require individuals to resolve competing demands, thereby placing pressure on control systems, with the anterior cingulate cortex (ACC) serving as a hub region for regulating control and monitoring uncertainty. Yet, ACC’s precise functional role remains debated. By systematically varying predictability and conflict, the conditions under which ACC activity adjusts to acute cognitive strain can be precisely examined. Extending beyond acute forms of strain, the symposium also considers how longer-lasting affective challenges influence brain structure. Structural MRI research on late-life depression examines subregion-specific vulnerability within the hippocampus, a structure that normally supports memory and learning. Comparisons between individuals with active versus remitted symptoms can further evaluate whether ongoing symptom persistence relates to differences in hippocampal integrity. Clarifying how the hippocampus is changing in response to long-term affective strain is important to advance our understanding of later-life vulnerability. Collectively, the research will demonstrate how physiological, cognitive, and affective strain influence network functional organisation, regional activity, and structural integrity. These perspectives will provide insight into the mechanisms that support adaptation, or reveal vulnerability, under diverse challenges. The symposium also offers a different angle for understanding mental health. By examining how the brain adjusts during physical challenge, demanding cognitive tasks, and persistent low mood, mental health is placed within the same scientific questions that guide work on neural function more broadly. This approach invites consideration of how different influences across life may relate to mental health and how this knowledge might inform future ways of supporting it.
10:30 Dr. Ala Yankouskaya
Bournemouth University, UK
"Cold-water immersion as a model of human adaptation: insights from brain, behaviour, and affect"
Acute physiological strain offers a uniquely tractable model for understanding how the human brain reorganises under pressure.
In this talk, I will present converging evidence from neuroimaging, electrophysiology, and large-scale behavioural data examining how brief cold-water immersion (CWI) influences affective state and neural function.
First, resting-state fMRI that even a 5-minute immersion triggers rapid reconfiguration of large-scale networks supporting self-referential processing, salience detection, and attentional control, with changes in connectivity closely paralleling shifts in positive and negative affect. New EEG findings extend this picture, showing immediate reductions in frontal alpha power and increased theta–beta coupling following CWI, biomarkers consistent with elevated vigilance, cognitive readiness, and improved mood regulation. Complementing the laboratory work, a large patient survey (N=700) reveals that individuals who regularly engage in cold-water practices report lower depressive symptoms, greater perceived stress resilience, and stronger beliefs in their ability to regulate mood, highlighting the broader psychosocial relevance of these physiological effects.
Together, these data suggest that acute cold exposure engages a multi-level adaptive response, spanning brain networks, electrophysiological dynamics, and subjective mood, that may help explain its emerging therapeutic potential.
11:10 Batuhan Serif Cakir
"The Function of Anterior Cingulate Cortex Under Cognitive Strain"
Bournemouth University, School of Psychology, Fern Barrow, BH12 5BB, Bournemouth, England
The anterior cingulate cortex (ACC) is central to monitoring control demands, signalling when situations generate cognitive strain, in the form of conflict or uncertainty. Based on the conflict monitoring account, the ACC detects response conflict when competing actions are activated, whereas task conflict theory argues that the ACC monitors competition between broader task sets.
By directly testing these competing predictions using a Stroop task, this work aims to clarify the ACC’s functional role.
Using fMRI, participants’ performance is measured across mixed blocks (containing equal proportions of congruent, incongruent, neutral, and letter-string trials, prompting high unpredictability) and pure blocks (each containing only one trial type; reducing cognitive demands).
Comparing ACC activity between pure versus mixed blocks, and across congruent, incongruent, neutral, and letter-string trials, allows a direct test of whether the ACC is activated primarily by response conflict, or by task-set conflict and unpredictability.
By outlining when and how the ACC is engaged, this talk will advance current discussions on its role in cognitive control and monitoring, contributing to ongoing debates about its function.
11:23 Brianca Renfro, MSc
Center for Cognitive Medicine, Department of Psychiatry and Behavioral Science, Vanderbilt University Medical Center, Nashville, TN, USA
"Hippocampal Total, Subregion, and Subfield Volume Alterations in Late-Life Depression"
Despite consistent support for smaller total hippocampal volumes in late-life depression (LLD), there is less consensus on LLD’s relationship with hippocampal subregions and subfields. This is particularly germane for interactive effects of aging in context of depression, as individuals with LLD may exhibit accelerated aging processes.
To investigate hippocampal total, subregion, and subfield volumes in LLD versus non-depressed controls and how age moderates these effects.
We examined 260 depressed and 140 non-depressed older adults who completed 3T MRI and extracted hippocampal subregion and subfield volumes. Primary analyses investigated effects of LLD diagnosis, active vs remitted depression, and age of onset on hippocampal volumes. Secondary analyses evaluated interactive effects of age and these diagnostic groupings on hippocampal volumes.
Compared to controls, the LLD group exhibited smaller total hippocampal volumes, with smaller volumes of the bilateral hippocampal head and the right hemisphere body, tail, CA1, and molecular layer. When comparing current and remitted LLD, individuals with current LLD exhibited smaller right total hippocampus, head, body, and molecular layer volumes compared to controls. They also exhibited smaller CA1, CA2, and CA4/dentate gyrus volumes compared to both control and remitted LLD groups. No regions differed between control and remitted LLD groups. We did not observe significant group differences in any volume measure between LLD individuals with an early- or later-life depression onset. There was no significant age by diagnostic group interactions on hippocampal volumes across any analyses.
This cross-sectional work supports diagnostic, but not accelerated aging, effects of depression on hippocampus volumes. In contrast to recently remitted LLD, currently depressed individuals exhibited smaller volumes primarily in the right hippocampus.
11:36 Mikołaj Compa
Institute of Psychology, Jagiellonian University, Krakow, Poland; Faculty of Psychology, SWPS University of Social Sciences and Humanities, Krakow, Poland
"Long-Term Exposure to Air Pollution Impacts Activity in Brain Regions Involved in Inhibitory Control in 10 to 13- Year Old Children"
The development of inhibitory control, a core component of cognitive control, can be influenced by environmental factors. We investigated whether exposure to particulate matter with diameter ≤ 10 μm (PM10) and nitrogen dioxide (NO2) across different life-time periods is related to the neural correlates of inhibitory control in 10- to 13-year-old children from southern Poland.
To investigate whether long-term exposure to air pollution is associated with task-related brain activity during inhibitory control, and to examine whether these associations differ between individuals with ADHD and typically developing peers.
Task functional magnetic resonance imaging (task fMRI) measures brain activity while participants perform specific cognitive or behavioral tasks. We investigated inhibition using a Go/NoGo task during task fMRI and tested associations between neural correlates of inhibitory control and exposure to air pollution during prenatal, early-life, and current life periods. The study population comprised children from the NeuroSmog study with Attention-Deficit/Hyperactivity Disorder (ADHD, n=143) and their typically developing peers (n = 385).
Higher current exposure to PM10 was significantly associated with reduced brain activation during response inhibition in key cognitive control networks, including the dorsolateral prefrontal cortex and anterior cingulate cortex. We did not observe significant interactions between our participants’ ADHD diagnosis and their exposure to air pollution.
Long-term exposure to air pollution was associated with impairments in brain function related to inhibition in both ADHD children and their typically developing peers. Our findings add novel, pertinent evidence to the growing body of research indicating that air pollution negatively impacts the development of executive function in children and suggests that the same mechanisms that underlie pollution’s effects on the brain may also lead to the increased incidence of ADHD.
11:49 Ruzanna A. Shushanyan
Research Institute of Biology, Department of Human and Animal Morphology and Physiology, Yerevan State University
"Visual System Vulnerability to Acute Hypoxia: Structural Remodelling and Pharmacological Modulation"
Acute exposure to hypoxic environments, such as high altitude, can lead to transient or lasting visual disturbances, including high-altitude retinopathy (HAR). These conditions arise from disrupted neurovascular regulation and impaired oxygen delivery to neural tissues. The retina is highly vulnerable to hypoxia, as is the visual cortex, making the visual system a sensitive readout of hypoxia-induced neurodegeneration.
In this study, we used a rat model of acute hypobaric hypoxia to examine how oxygen deprivation alters retinal cytoarchitecture and neurovascular integrity, and whether corticosteroid intervention can modify these effects.
Animals were exposed to a simulated high altitude environment, with a subset receiving dexamethasone pretreatment. Hypoxic injury was induced in a hypobaric chamber (FiO₂ = 16.6%) for 6 hours/day over 3 days. Animals in the treatment group received a single intraperitoneal dose of dexamethasone (1 mg/kg) before hypoxic exposure. Histomorphological and ultrastructural analyses have been utilized to reveal hypoxia-associated cellular injury and the modulatory effect of the corticosteriod pretreatment.
Hypoxic exposure resulted in marked structural remodeling of the inner retina, including thickening of the ganglion cell and nerve fiber layers, vascular leakage, and neuronal swelling, accompanied by degenerative changes in the visual cortex. In contrast, dexamethasone pretreatment attenuated inflammatory responses, preserved barrier integrity, and maintained retinal and cortical neuronal organization.
These findings demonstrate that acute hypoxia rapidly reshapes retinal structure through inflammatory and neurovascular mechanisms, and that pharmacological modulation can partially restore neural integrity. HAR may therefore provide a useful experimental framework for studying hypoxia-driven neurodegeneration across the visual system.
Chairman: Marianna Constantinou
