Nature and Nurture: Brain Region-Specific Inheritance of Sleep Neurophysiology in Adolescence

Abstract

Sleep-specific oscillations of spindles and slow waves are generated through thalamocortical and corticocortical loops, respectively, and provide a unique opportunity to measure the integrity of these neuronal systems. Understanding the relative contribution of genetic factors to sleep oscillations is important for determining whether they constitute useful endophenotypes that mark vulnerability to psychiatric illness. Using high-density sleep EEG recordings in human adolescent twin pairs (n ϭ 60; 28 females), we find that over posterior regions 80-90% of the variance in slow oscillations, slow wave, and spindle activity is due to genes. Surprisingly, slow (10-12 Hz) and fast (12-16 Hz) anterior spindle amplitude and power are largely driven by environmental factors shared among the twins. To our knowledge this is the first example of a neural phenotype that exhibits a strong influence of nature in one brain region, and nurture in another. Overall, our findings highlight the utility of the sleep EEG as a reliable and easy to measure endophenotype during adolescence. This measure may be used to measure disease risk in development before the onset of a psychiatric disorder; the location within the brain of deficits in sleep neurophysiology may suggest whether the ultimate cause is genetic or environmental.

Association between depressive symptoms and sleep neurophysiology in early adolescence

“…Fifty‐two healthy adolescents (mean age: 12.31 years; SD : 1.121; 25 female) were recruited through flyers and contact with parent groups as part of a twin study aiming to investigate the genetic influence on adolescent sleep (Markovic, Achermann, Rusterholz, & Tarokh, ; Rusterholz et al., ). Participants with a personal history of chronic or current disease were excluded as were individuals born severely preterm (<30th gestation week) as determined via telephone contact with parents.…”

<p>Healthy Eating, Physical Activity, and Sleep Hygiene (HEPAS) as the Winning Triad for Sustaining Physical and Mental Health in Patients at Risk for or with Neuropsychiatric Disorders: Considerations for Clinical Practice</p>

“…Sleep changes are often the earliest signs of several neuropsychiatric disorders, but have also been considered as state markers for mental illnesses, partly as our genetic makeup. 6 For the purpose of the present overview, data from Google Scholar, PubMed, and Scopus databases were searched and reviewed, focusing on publications regarding diet, physical fitness, and sleeping patterns in the prevention and overall management of neuropsychiatric disorders, mainly encompassing schizophrenia spectrum disorders, mood disorders, anxiety disorders, and neurocognitive disorders. The search considered relevant studies to introduce the rationale for each section and discuss retrospective and prospective clinical trials, systematic and non-systematic reviews, meta-analyses, guidelines and expert opinions.…”

Heterogeneous profiles of coupled sleep oscillations in human hippocampus

“…Nonetheless, we emphasize that this group-level conclusion does not reflect individual patients, who showed marked differences in spectral power and PAC along the HPC axis. We suggest that individual differences in HPC PAC constitute true variability representative of the population, similar to replicable individual differences of scalp sleep oscillations (25,(52)(53)(54)(55). Whether such variability is further related to general (e.g., cognitive functioning, age) or disease-related (e.g., epilepsy history, medication) factors cannot be determined from the present sample.…”

“…Given that sleep oscillations are often spatially restricted (20,24,25,51), it is an open question whether these rhythms and their interactions vary along the longitudinal axis of the human HPC, possibly in relation to functional specialization. Another relevant factor concerns between-subject variability, with various aspects of scalp-recorded sleep oscillations showing large and reproducible individual differences (25,(52)(53)(54)(55). Whether such variability extends to human HPC is unknown.…”