Why do many psychiatric disorders emerge during adolescence?

Paus, Tomáš; Keshavan, Matcheri S.; Giedd, Jay N.

doi:10.1038/nrn2513

Cited by 2,619 publications

(2,022 citation statements)

References 106 publications

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“…State independent, general mechanisms are also implicated by the fact that global EEG power decrease parallels maturational trajectories in sleep (Buchmann et al, 2011) and awake resting state (Whitford et al, 2007). Gray matter decrease reflects synaptic pruning (Bourgeois and Rakic, 1993;Huttenlocher, 1979), which presumably eliminates redundant connections and may be disrupted in adolescent psychiatric diseases (Paus et al, 2008). Physiologically, synaptic density may affect EEG power, as synaptic density reflects the connectivity and size of neuron populations from which EEG power partly derives (Boord et al, 2007;Feinberg and Campbell, 2010).…”

Section: Introductionmentioning

confidence: 99%

Brain state regulation during normal development: Intrinsic activity fluctuations in simultaneous EEG–fMRI

et al. 2012

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Brain maturation in adolescence is mirrored by the EEG as a pronounced decrease in low frequency activity. This EEG power attenuation parallels reductions of structural and metabolic markers of neuronal maturation (i.e., gray matter loss and decrease of absolute cerebral glucose utilization). However, it is largely unknown what causes these electrophysiological changes, and how this functional reorganization relates to other functional measures such as the fMRI BOLD signal. In this study, we used simultaneously recorded EEG and fMRI to localize hemodynamic correlates of fluctuating EEG oscillations and to study the development of this EEG-BOLD coupling. Furthermore, the maturational EEG power attenuation was directly compared to BOLD signal power maturation. Both analyses were novel in their developmental perspective and aimed at providing a functional lead to EEG maturation. Data from 19 children, 18 adolescents and 18 young adults were acquired in 10min eyes-open/eyes-closed resting states. Our results revealed that both EEG and BOLD amplitudes strongly decrease between childhood and adulthood, but their functional coupling remains largely unchanged. The global reduction of absolute amplitude of spontaneous slow BOLD signal fluctuation is a novel marker for brain maturation, and parallels the globally decreasing trajectories of EEG amplitudes, gray matter and glucose metabolism during adolescence. Further, the absence of thalamocortical EEG-BOLD coupling in children together with age-related normalized thalamic BOLD power increase indicated maturational changes in brain state regulation. Abstract -Brain maturation in adolescence is mirrored by the EEG as a pronounced decrease in low frequency activity. This EEG power attenuation parallels reductions of structural and metabolic markers of neuronal maturation (i.e., gray matter loss and decrease of absolute cerebral glucose utilization). However, it is largely unknown what causes these electrophysiological changes, and how this functional reorganization relates to other functional measures such as the fMRI BOLD signal. In this study, we used simultaneously recorded EEG and fMRI to localize hemodynamic correlates of fluctuating EEG oscillations and to study the development of this EEG-BOLD coupling. Furthermore, the maturational EEG power attenuation was directly compared to BOLD signal power maturation. Both analyses were novel in their developmental perspective and aimed at providing a functional lead to EEG maturation. Data from 19 children, 18 adolescents and 18 young adults were acquired in 10 min eyes-open/eyes-closed resting states. Our results revealed that both EEG and BOLD amplitudes strongly decrease between childhood and adulthood, but their functional coupling remains largely unchanged. The global reduction of absolute amplitude of spontaneous slow BOLD signal fluctuation is a novel marker for brain maturation, and parallels the globally decreasing trajectories of EEG amplitudes, gray matter and glucose metabolism during adolescence. Furthe...

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Section: Introductionmentioning

confidence: 99%

Brain state regulation during normal development: Intrinsic activity fluctuations in simultaneous EEG–fMRI

et al. 2012

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“…It is well known that adolescence is a period of important social, neurobiological, and behavioral changes (Paus et al, 2008). As a consequence, the etiology of sleep duration might change throughout adolescence.…”

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Genetic and Environmental Influences on Individual Differences in Sleep Duration During Adolescence

Velde

Boomsma

et al. 2013

Twin Res Hum Genet

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This study assessed to what extent genetic and environmental factors contributed to individual differences in adolescent sleep duration, and whether genetic and environmental contributions to sleep duration changed throughout adolescence. A twin-family design was used to gain insight into the genetic and environmental contributions to variation in sleep duration. The study sample consisted of 6,319 adolescent twins (44% males) and 1,359 non-twin siblings (44% males) in the age range of 12 to 20 years (mean age = 16.85, SD = 1.40). The participants self-reported usual sleep duration, which was categorized as less than 8 hours per night, 8-9 hours per night, and more than 9 hours per night. Results showed that the prevalence of shorter than optimum sleep duration, that is, less than 8 hours per night, was high, with the highest prevalence rates in later adolescence. The contribution of genetic and environmental factors to individual differences in sleep duration was dependent on age. Variation in sleep duration at the age of 12 years was accounted for by genetic (boys: 34%, girls: 36%), shared environmental (boys: 28%, girls: 45%), and non-shared environmental factors (boys: 38%, girls: 19%). At the age of 20 years, the role of genetic (boys: 47%, girls: 33%) and non-shared environmental factors (boys: 53%, girls: 67%) was more pronounced. It can be concluded from the results that individual differences in sleep duration were accounted for by genetic and non-shared environmental factors throughout adolescence, whereas shared environmental factors account for a substantial part of variation during early adolescence only.

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“…These techniques have initiated a new field of research on the neurobiology of the adolescent brain. Gaining insight into the maturational processes that take place during this period of brain development, and into the etiology of individual differences in these processes, will aid in understanding the development of psychiatric disorders, since many psychiatric disorders become apparent around or right after puberty (Kessler et al, 2007;Paus et al, 2008).…”

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Brain SCALE: Brain Structure and Cognition: an Adolescent Longitudinal Twin Study into the Genetic Etiology of Individual Differences

et al. 2012

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From childhood into adolescence, the child's brain undergoes considerable changes in both structure and function. Twin studies are of great value to explore to what extent genetic and environmental factors explain individual differences in brain development and cognition. In The Netherlands, we initiated a longitudinal study in which twins, their siblings and their parents are assessed at three year intervals. The participants were recruited from The Netherlands Twin Register (NTR) and at baseline consisted of 112 families, with 9-year-old twins and an older sibling. Three years later, 89 families returned for follow-up assessment. Data collection included psychometric IQ tests, a comprehensive neuropsychological testing protocol, and parental and self-ratings of behavioral and emotional problems. Physical maturation was measured through assessment of Tanner stages. Hormonal levels (cortisol, luteinizing hormone, follicle-stimulating hormone, testosterone, and estrogens) were assessed in urine and saliva. Brain scans were acquired using 1.5 Tesla Magnetic Resonance Imaging (MRI), which provided volumetric measures and measures of cortical thickness. Buccal swabs were collected for DNA isolation for future candidate gene and genomewide analysis studies. This article gives an overview of the study and the main findings. Participants will return for a third assessment when the twins are around 16 years old. Longitudinal twin-sibling studies that map brain development and cognitive function at well-defined ages aid in the understanding of genetic influences on normative brain development.

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Why do many psychiatric disorders emerge during adolescence?

Cited by 2,619 publications

References 106 publications

Brain state regulation during normal development: Intrinsic activity fluctuations in simultaneous EEG–fMRI

Brain state regulation during normal development: Intrinsic activity fluctuations in simultaneous EEG–fMRI

Genetic and Environmental Influences on Individual Differences in Sleep Duration During Adolescence

Brain SCALE: Brain Structure and Cognition: an Adolescent Longitudinal Twin Study into the Genetic Etiology of Individual Differences

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