V-088
Aging disrupts the temporal organization of slow oscillations beyond density reduction
Lucila Capurro1, Michael Radloff2, María C. González1, María L. Gorosito1, Luis I. Brusco3,4, Rodrigo Ramele5, Cecilia Forcato1
  1. Laboratorio de Sueño y Memoria, Departamento de Ciencias de la Vida, Instituto Tecnológico de Buenos Aires (ITBA), Ciudad Autónoma de Buenos Aires, Argentina
  2. Department of Health Psychology, Institute for Psychology, University of Klagenfurt, Klagenfurt, Austria
  3. Centro de Neuropsiquiatría y Neurología de la Conducta-CENECON, Facultad de Ciencias Médicas, Universidad de Buenos Aires (UBA), Ciudad Autónoma de Buenos Aires, Argentina
  4. Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), Ciudad Autónoma de Buenos Aires, Argentina
  5. Departamento de Ingeniería Informática, Instituto Tecnológico de Buenos Aires (ITBA), Ciudad Autónoma de Buenos Aires, Argentina
Presenting Author:
Lucila Capurro
lcapurro@itba.edu.ar
Sleep slow oscillations (SOs) are a hallmark of NREM sleep and play a crucial role in glymphatic clearance. Age-related reductions in SO density and amplitude are well documented and linked to impaired clearance. However, little is known about whether aging also alters their temporal organization. In this work, we introduce a novel approach to classify SOs according to their temporal structure, distinguishing isolated SOs from trains of consecutive SOs based on inter-SO intervals. We analyzed overnight EEG recordings from 57 young and 51 elderly adults across three independent datasets. We quantified the proportion of isolated versus consecutive SOs and examined the distribution of train lengths. Elderly adults showed a significantly higher proportion of isolated SOs and shorter trains compared to young adults. These effects remained robust after controlling for SO density and sleep stage composition. Additional analyses using temporal shuffling and density-matched epochs confirmed that the observed differences cannot be explained solely by lower SO density, but rather reflect a genuine age-related loss of rhythmicity. These findings reveal that natural aging disrupts not only the amount and amplitude of SOs but also their temporal regularity. Such temporal disorganization may weaken sustained ionic currents underlying CSF flow, reduce the efficiency of metabolic waste clearance during sleep, and contribute to increased vulnerability to neurodegenerative processes.