The midpoint of cortical thinning between late childhood and early adulthood differs between individuals and brain regions: Evidence from longitudinal modelling in a 12-wave neuroimaging sample

Fuhrmann, Delia; Madsen, Kathrine Skak; Johansen, Louise Baruël; Baaré, William Frans Christiaan; Kievit, Rogier A.

doi:10.1101/2022.02.10.479868

Cited by 14 publications

(18 citation statements)

References 72 publications

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“…These results indicate that PFC volume is affected in a sex-specific manner, and that there are differences in consequences between episodes of binge drinking and the progression to AUD. Normal cortical thinning patterns throughout adolescence show different rates of cortical thinning across region and during various timepoints of adolescence ( Fuhrmann et al, 2022 ), suggesting that the age at which an individual begins binge drinking may have differing effects on cortical development. Fuhrmann et al (2022) identified the midpoint of cortical thinning (MCT) (i.e., the point at which the cortex thins fastest) to be around 15 years of age, with more frontal regions (such as the frontal gyrus) reaching MCT earlier (around age 14) while cingulate regions reached MCT later (around age 17).…”

Section: Human Studies Of Alcohol Exposurementioning

confidence: 99%

“…Normal cortical thinning patterns throughout adolescence show different rates of cortical thinning across region and during various timepoints of adolescence ( Fuhrmann et al, 2022 ), suggesting that the age at which an individual begins binge drinking may have differing effects on cortical development. Fuhrmann et al (2022) identified the midpoint of cortical thinning (MCT) (i.e., the point at which the cortex thins fastest) to be around 15 years of age, with more frontal regions (such as the frontal gyrus) reaching MCT earlier (around age 14) while cingulate regions reached MCT later (around age 17). The cortical alterations seen in these studies may be representative of differing cortical changes across the development of AUD in the two sexes and highlights the need for precise reporting and tracking in cortical subregions.…”

Section: Human Studies Of Alcohol Exposurementioning

confidence: 99%

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Adolescent Alcohol and Stress Exposure Rewires Key Cortical Neurocircuitry

et al. 2022

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Human adolescence is a period of development characterized by wide ranging emotions and behavioral risk taking, including binge drinking (Konrad et al., 2013). These behavioral manifestations of adolescence are complemented by growth in the neuroarchitecture of the brain, including synaptic pruning (Spear, 2013) and increases in overall white matter volume (Perrin et al., 2008). During this period of profound physiological maturation, the adolescent brain has a unique vulnerability to negative perturbations. Alcohol consumption and stress exposure, both of which are heightened during adolescence, can individually and synergistically alter these neurodevelopmental trajectories in positive and negative ways (conferring both resiliency and susceptibility) and influence already changing neurotransmitter systems and circuits. Importantly, the literature is rapidly changing and evolving in our understanding of basal sex differences in the brain, as well as the interaction between biological sex and life experiences. The animal literature provides the distinctive opportunity to explore sex-specific stress- and alcohol- induced changes in neurocircuits on a relatively rapid time scale. In addition, animal models allow for the investigation of individual neurons and signaling molecules otherwise inaccessible in the human brain. Here, we review the human and rodent literature with a focus on cortical development, neurotransmitters, peptides, and steroids, to characterize the field’s current understanding of the interaction between adolescence, biological sex, and exposure to stress and alcohol.

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Section: Human Studies Of Alcohol Exposurementioning

confidence: 99%

Section: Human Studies Of Alcohol Exposurementioning

confidence: 99%

Adolescent Alcohol and Stress Exposure Rewires Key Cortical Neurocircuitry

et al. 2022

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“…After birth, our brains continue to grow and change for much of our lives; typically, our brains are ~80% of the maximum size by age 3, with the maximum gray matter, subcortical gray, and white matter volumes reached by age 6, 14, and 30, respectively (Bethlehem et al, 2022). After maximum brain volume is reached, regional declines are observed with age and each region exhibits a different rate of volume decline (Ziegler et al, 2012;Tamnes et al, 2013;Fuhrmann et al, 2022). After age 40 the volume of brain ventricles begins to rapidly increase, and after age 50 the white matter volume rapidly declines with age (Bethlehem et al, 2022).…”

Section: Heads: Age Impacts Neurotoxic Effects Of Chemicalsmentioning

confidence: 99%

The intersection between toxicology and aging research: A toxic aging coin perspective

Wise

2022

Front. Aging

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We are imminently faced with the challenges of an increasingly aging population and longer lifespans due to improved health care. Concomitantly, we are faced with ubiquitous environmental pollution linked with various health effects and age-related diseases which contribute to increased morbidity with age. Geriatric populations are rarely considered in the development of environmental regulations or in toxicology research. Today, life expectancy is often into one’s 80s or beyond, which means multiple decades living as a geriatric individual. Hence, adverse health effects and late-onset diseases might be due to environmental exposures as a geriatric, and we currently have no way of knowing. Considering aging from a different perspective, the term “gerontogen” was coined in 1987 to describe chemicals that accelerate biological aging but has largely been left out of toxicology research. Thus, we are challenged with a two-faced problem that we can describe as a “toxic aging coin”; on one side we consider how age affects the toxic outcome of chemicals, whereas on the other side we consider how chemicals accelerate aging (i.e. how chemicals act as gerontogens). Conveniently, both sides of this coin can be tackled with a single animal study that considers multiple age groups and assesses basic toxicology of the chemical(s) tested and aging-focused endpoints. Here, I introduce the concept of this toxic aging coin and some key considerations for how it applies to toxicology research. My discussion of this concept will focus on the brain, my area of expertise, but could be translated to any organ system.

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“…Over the past decades, progress has been made toward understanding how the anatomy of the cerebral cortex broadly changes during human development. For example, prior work has shown that cortical gray matter decreases while cortical white matter and surface area increase (Gogtay et al, 2004; Sowell et al, 2004; Lebel et al, 2008; Shaw et al, 2008; Brown et al, 2012; Amlien et al, 2016; Tamnes et al, 2017; de Faria et al, 2021; Norbom et al, 2021; Baum et al, 2022; Bethlehem et al, 2022; Fuhrmann et al, 2022). Nevertheless, a critical gap in knowledge remains: How do neuroanatomical structures within the cerebral cortex—especially those that are hominoid-specific—develop at the individual level?…”

Section: Introductionmentioning

confidence: 99%

Development of human lateral prefrontal sulcal morphology and its relation to reasoning performance

Willbrand

Ferrer

Bunge

et al. 2022

Preprint

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Previous findings show that the morphology of folds (sulci) of the human cerebral cortex flatten during postnatal development. However, previous studies did not consider the relationship between sulcal morphology and cognitive development in individual participants. Here, we fill this gap in knowledge by leveraging cross-sectional morphological neuroimaging data in the lateral prefrontal cortex (LPFC) from individual human participants (6-36 years old, males and females; N = 108; 3672 sulci), as well as longitudinal morphological and behavioral data from a subset of child and adolescent participants scanned at two timepoints (6-18 years old; N = 44; 2992 sulci). Manually defining thousands of sulci revealed that LPFC sulcal morphology (depth, surface area, gray matter thickness, and local gyrification index) differed between children (6-11 years old)/adolescents (11-18 years old) and young adults (22-36 years old) cross-sectionally, but only cortical thickness showed both cross-sectional differences between children and adolescents and presented longitudinal changes during childhood and adolescence. Furthermore, a data-driven approach relating morphology and cognition identified that longitudinal changes in cortical thickness of four rostral LPFC sulci predicted longitudinal changes in reasoning performance, a higher-level cognitive ability that relies on LPFC. Contrary to previous findings, these results suggest that sulci may flatten either after this time frame or over a longer longitudinal period of time than previously presented. Crucially, these results also suggest that longitudinal changes in the cortex within specific LPFC sulci are behaviorally meaningful, providing targeted structures, and areas of the cortex, for future neuroimaging studies examining the development of cognitive abilities.

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The midpoint of cortical thinning between late childhood and early adulthood differs between individuals and brain regions: Evidence from longitudinal modelling in a 12-wave neuroimaging sample

Cited by 14 publications

References 72 publications

Adolescent Alcohol and Stress Exposure Rewires Key Cortical Neurocircuitry

Adolescent Alcohol and Stress Exposure Rewires Key Cortical Neurocircuitry

The intersection between toxicology and aging research: A toxic aging coin perspective

Development of human lateral prefrontal sulcal morphology and its relation to reasoning performance

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