Biology subjects

Riedner, B. A.

Publications and source records attributed to Riedner, B. A..

3 recordsLinked to original sources

bioRxiv2026

Longitudinal Alterations in Sleep EEG Biomarkers of Memory Consolidation in Middle-Aged and Older Adults

The precise coordination of slow oscillations (SO) and sleep spindles during non-rapid eye movement (NREM) sleep supports memory consolidation and may serve as a sensitive marker of cognitive aging. However, longitudinal changes in their oscillatory dynamics in midlife and older age remain poorly understood. Using polysomnography with high-density EEG at two timepoints over [~]2.5 years, we examined changes in local NREM slow wave (SW), sleep spindle (occurring in the 11-16 Hz sigma range), and SO-sigma coupling strength in cognitively unimpaired middle-aged to older adults at risk for Alzheimers disease. Fronto-central SO-sigma power coupling strength significantly declined over time, independent of changes in multiple measures of SW and sleep spindle expression. Local declines in multiple sleep spindle measures were also observed. Greater baseline levels of cerebrospinal fluid (CSF) neurogranin, a postsynaptic protein abundantly expressed in the dendritic spines of the hippocampus and cerebral cortex and implicated in calcium-dependent synaptic plasticity, predicted the magnitude of longitudinal decline in SO-fast sigma coupling strength, which in turn predicted episodic memory performance changes. These findings suggest that longitudinal changes in local sleep oscillatory dynamics are related to decreased synaptic integrity and may serve as an early indicator of memory decline in older adults at risk for Alzheimers disease.

neuroscience↗

bioRxiv2025

Electrophysiological effects of psilocybin co-administered with midazolam

The serotonergic psychedelic psilocybin induces neural plasticity and profoundly alters consciousness. The benzodiazepine midazolam blunts neural plasticity and induces conscious sedation and amnesia at low doses. In our recent open label pilot study, we administered oral psilocybin (25 mg) along with intravenous midazolam at doses allowing a full psychedelic experience while blunting memory for the experience. We previously reported preliminary results from high density scalp electroencephalography (EEG) recorded during the dosing session. Here, we examined changes in EEG band power, normalized Lempel Ziv complexity (LZCn), and spectral exponent. We used linear mixed effects models that incorporated time and the subjective effects of midazolam and psilocybin, measured with the Observers Assessment of Arousal and Sedation (OAA/S) and selected items from the Altered States of Consciousness (ASC) questionnaire, respectively. At 15-30 mins, when midazolam (but likely not psilocybin) was at its targeted effect site concentration, we observed increased beta power and decreased spectral exponent. As the subjective effects of psilocybin commenced and over the next six hours, we observed increased LZCn and spectral exponent and decreased broadband power. OAA/S improved model fits for alpha power while ASC improved model fits for LZCn and spectral exponent. These data are further evidence that the effects of psilocybin are maintained in the presence of midazolam, supporting its utility in mechanistic studies of psilocybins therapeutic activity.

neuroscience↗

bioRxiv2019

Integrity of corpus callosum is essential for the cross-hemispheric propagation of sleep slow waves: a high-density EEG study in split-brain patients

The slow waves of NREM-sleep (0.5-4Hz) reflect experience-dependent plasticity and play a direct role in the restorative functions of sleep. Importantly, slow waves behave as traveling waves and their propagation is assumed to reflect the structural properties of white matter connections. Based on this assumption, the corpus callosum (CC) may represent the main responsible for cross-hemispheric slow wave propagation. To verify this hypothesis, here we studied a group of patients who underwent total callosotomy due to drug-resistant epilepsy. Overnight high-density (hd)-EEG recordings (256 electrodes) were performed in five totally callosotomized in-patients (CP; 40-53y, 2F), in three control non-callosotomized neurological in-patients (NP; 44-66y, 2F, 1M epileptic), and in an additional sample of 24 healthy adult subjects (HS; 20-47y, 13F). Data were inspected to select NREM-sleep epochs and artefactual or non-physiological activity was rejected. Slow waves were detected using an automated algorithm and their properties and propagation patterns were computed. For each slow wave parameter and for each patient, the relative z-score and the corresponding p-value were calculated with respect to the distribution represented by the HS-group. Group differences were considered significant only when a Bonferroni corrected P < 0.05 was observed in all the CP and in none of the NP. A regression-based adjustment was used to exclude potential confounding effects of age. Slow wave density, amplitude, slope and propagation speed did not differ across CP and HS. In all CP slow waves displayed a significantly reduced probability of cross-hemispheric propagation and a stronger inter-hemispheric asymmetry. Moreover, we found that the incidence of large slow waves tended to differ across hemispheres within individual NREM epochs, with a relative predominance of the right over the left hemisphere in both CP and HS. The absolute magnitude of this inter-hemispheric difference was significantly greater in CP relative to HS. This effect did not depend on differences in slow wave origin within each hemisphere across groups. Present results indicate that the integrity of the CC is essential for the cross-hemispheric traveling of sleep slow waves, supporting the assumption of a direct relationship between white matter structural integrity and cross-hemispheric slow wave propagation. Our findings also imply a prominent role of cortico-cortical connections, rather than cortico-subcortico-cortical loops, in slow wave cross-hemispheric synchronization. Finally, this data indicate that the lack of the CC does not lead to differences in sleep depth, in terms of slow wave generation/origin, across brain hemispheres.

neuroscience↗