Francisco Zamorano

Background: Sedentarism is prevalent and associated with poorer mental and physical health. Whether everyday physical activity (PA) maps onto computational decision strategies and brain structure/function in non-elderly adults remains unclear. Methods: Seventy-one healthy adults (39 women; 18–45 years) completed the Multi-Source Interference Task (MSIT) during fMRI. PA was quantified with the short IPAQ and participants were classified as Active or Sedentary. Behavior (RT, accuracy) was analyzed with frequentist models and a hierarchical Bayesian drift–diffusion model (DDM) estimating drift rate ( v ), boundary separation ( α ), and non-decision time (τ). First-level fMRI modeled congruent/incongruent trials; group-level analyses used FLAME1 with cluster-wise FWE correction (z>3.1, p <.05). Structural MRI was processed with FreeSurfer 7.4.1 (cortical thickness, hippocampal subfields); surface-based GLMs tested group and DDM effects. Results: Active participants responded faster overall; incongruent accuracy showed a speed– accuracy trade-off (accuracy increased with slower RTs), with a significant RT × group interaction. In the DDM, boundary separation ( α ) was higher in sedentary individuals (greater caution), whereas drift rate ( v ) differed by sex (males > females). Structurally, the active group showed larger left hippocampal subfields and thicker cortex in posterior temporal & anterior cingulate regions that are negatively related to α . Functionally, boundary-related BOLD modulation encompassed fusiform, posterior cingulate, superior temporal cortex, and SMA; Active > Sedentary contrasts highlighted left occipital and inferior parietal lobe. Conclusions: Everyday PA aligns with lower decision thresholds, select structural advantages, and more efficient task-engaged networks, suggesting PA fosters adaptive, resource-efficient cognitive control. These mechanistic links support PA-based strategies to mitigate risks of sedentarism.

Persistent cognitive symptoms following SARS-CoV-2 infection have been widely reported, yet their underlying neural mechanisms remain poorly understood. Here, we applied an integrative framework—combining EEG, diffusion MRI, and computational cognitive modeling—to investigate brain–behavior relationships in patients recovered from COVID-19 (n=70) and other non-COVID respiratory infections (n=26). Participants completed tasks probing cognitive control, working memory, and decision-making. Across tasks, individuals with prior COVID-19 showed altered low-frequency oscillatory activity and performance deficits, despite mild or moderate acute illness. These oscillatory alterations were linked to reduced white matter integrity in distinct long-range tracts, including the cingulum and thalamo-occipital fasciculi, depending on the cognitive computation involved. Crucially, model-based clustering revealed two distinct neurophysiological profiles among post-COVID participants, reflecting different combinations of structural and functional alterations. These profiles were not explained by clinical severity markers or other symptoms like anosmia, suggesting the emergence of neurocognitive phenotypes beyond binary classifications. Our findings identify a generalizable principle whereby specific brain network disruptions underlie cognitive dysfunction, highlighting biomarkers that may guide personalized intervention strategies. Beyond COVID-19, this multimodal framework offers a scalable approach for uncovering structure–function–computation coupling in other post-infectious or neuroinflammatory conditions, with broad relevance for the prevention and treatment of cognitive impairment.

(1) Background: Persistent postural-perceptual dizziness (PPPD) is a common chronic dizziness disorder with an unclear pathophysiology. It is hypothesized that PPPD may involve disrupted spatial cognition processes as a core feature. (2) Methods: A cohort of 19 PPPD patients underwent psycho-cognitive testing, including assessments for anxiety, depression, memory, attention, planning, and executive functions, with an emphasis on spatial navigation via a virtual Morris water maze. These patients were compared with 12 healthy controls and 20 individuals with other vestibular disorders but without PPPD. Vestibular function was evaluated using video head impulse testing and vestibular evoked myogenic potentials, while brain magnetic resonance imaging was used to exclude confounding pathology. (3) Results: PPPD patients demonstrated unique impairments in allocentric spatial navigation (as evidenced by the virtual Morris water maze) and in other high-demand visuospatial cognitive tasks that involve executive functions and planning, such as the Towers of London and Trail Making B tests. A factor analysis highlighted spatial navigation and advanced visuospatial functions as being central to PPPD, with a strong correlation to symptom severity. (4) Conclusions: PPPD may broadly impair higher cognitive functions, especially in spatial cognition. We discuss a disruption in the creation of enriched cognitive spatial maps as a possible pathophysiology for PPPD.