When Maturation is Not Linear: Brain Oscillatory Activity in the Process of Aging as Measured by Electrophysiology.

Changes in brain oscillatory activity are commonly used as biomarkers both in cognitive neuroscience and in neuropsychiatric conditions. However, little is known about how its profile changes across maturation. Here we use regression models to characterize magnetoencephalography power changes within classical frequency bands in a sample of 792 healthy participants, covering the range 13 to 80 years old. Our findings unveil complex, non-linear power trajectories that defy the traditional linear paradigm, with notable cortical region variations. Interestingly, slow wave activity increases correlate with improved cognitive performance throughout life and larger gray matter volume in the elderly. Conversely, fast wave activity diminishes in adulthood. Elevated low-frequency activity during aging, traditionally seen as compensatory, may also signify neural deterioration. This dual interpretation, highlighted by our study, reveals the intricate dynamics between brain oscillations, cognitive performance, and aging. It advances our understanding of neurodevelopment and aging by emphasizing the regional specificity and complexity of brain rhythm changes, with implications for cognitive and structural integrity.

Dropping mortality by increasing connectivity in plant epidemics.

Pathogen introduction in plant communities can cause serious impacts and biodiversity losses that may take a long time to manage and restore. Effective control of epidemic spreading in the wild is a problem of paramount importance because of its implications in conservation and potential economic losses. Understanding the mechanisms that hinder pathogen propagation is, therefore, crucial. Usual modelization approaches in epidemic spreading are based in compartmentalized models, without keeping track of pathogen concentrations during spreading. In this contribution we present and fully analyze a dynamical model for plant epidemic spreading based on pathogen abundances. The model, which is defined on top of network substrates, is amenable to a deep mathematical analysis in the absence of a limit in the amount of pathogen a plant can tolerate before dying. In the presence of such death threshold, we observe that the fraction of dead plants peaks at intermediate values of network connectivity, and mortality decreases for large average degrees. We discuss the implications of our results as mechanisms to halt infection propagation.