Development of cortical folding during evolution and ontogeny

Zilles, Karl; Palomero‐Gallagher, Nicola; Amunts, Katrin

doi:10.1016/j.tins.2013.01.006

Cited by 473 publications

(474 citation statements)

References 88 publications

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“…We found that each scaling relationship could be explained comparably well by either a non-linear function ( Figure 3A) or two grade-shifted linear functions, with the best-fit linear models drawing significantly different slopes for high-GI and low-GI species ( Figure 3B-3D Figure 3D), thus providing a neuron number correlate for the GI threshold. The deviation of these results from previous work, which have shown strong phylogenetic signals associated with both GI [31,32] and neuron counts [33], may be explained both by our more than 2-fold increase in sampled species and the a priori assumption of previous work that GI and neuron number evolve as a function of phylogeny. Variation in GI, therefore, has not evolved linearly across the phylogeny, but has in fact been differentially evolved in two phenotypic groups.…”

Section: A Neocortical Threshold Gicontrasting

confidence: 92%

An Adaptive Threshold in Mammalian Neocortical Evolution

Lewitus

Kelava

Kalinka

et al. 2013

Preprint

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Expansion of the neocortex is a hallmark of human evolution. However, determining which adaptive mechanisms facilitated its expansion remains an open question. Here we show, using the gyrencephaly index (GI) and other physiological and lifehistory data for 102 mammalian species, that gyrencephaly is an ancestral mammalian trait. We find that variation in GI does not evolve linearly across species, but that mammals constitute two principal groups above and below a GI threshold value of 1.5, approximately equal to 10 9 neurons, which may be characterized by distinct constellations of physiological and lifehistory traits. By integrating data on neurogenic period, neuroepithelial founder pool size, cell-cycle length, progenitor-type abundances, and cortical neuron number into discrete mathematical models, we identify symmetric proliferative divisions of basal progenitors in the subventricular zone of the developing neocortex as evolutionarily necessary for generating a 14-fold increase in daily prenatal neuron production, traversal of the GI threshold, and thus establishment of two principal groups. We conclude that, despite considerable neuroanatomical differences, changes in the length of the neurogenic period alone, rather than any novel neurogenic progenitor lineage, are sufficient to explain differences in neuron number and neocortical size between species within the same principal group.

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Section: A Neocortical Threshold Gicontrasting

confidence: 92%

An Adaptive Threshold in Mammalian Neocortical Evolution

Lewitus

Kelava

Kalinka

et al. 2013

Preprint

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“…27 According to previous studies, gyrification reaches its developmental peak before early toddlerhood. [33][34][35] Therefore, variations in gyrification are often discussed as useful markers for processes that evolved during a crucial period of early brain development.…”

Section: Comparison With Surface-based Studiesmentioning

confidence: 99%

Structural alterations in patients with obsessive–compulsive disorder: a surface-based analysis of cortical volume, surface area and thickness

Rus

Reeß

Wagner

et al. 2017

JPN

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IntroductionStudying the brain anatomic structure offers a promising approach to improve our understanding of neural functional alter ations often encountered in individuals with psychiatric disorders. In those with obsessive-compulsive disorder (OCD), a psychiatric disorder with a 2%-3% lifetime prevalence 1 that causes strong impairment of daily life, findings up to now show disruptions on a functional and a structural neural level, mainly in a network including cortico-striatothalamo-cortical (CSTC) areas. Overall, these findings are rather inconsistent and limited by confounding factors, such as differences in clinical characteristics of the study sample or varying methodological approaches.Meta-analytic reviews showed that cortical areas, mainly the anterior cingulate cortex (ACC), orbitofrontal cortex (OFC) and parietofrontal regions, seem to be predominantly affected by grey matter volume deficits in patients with OCD, whereas the lenticular nuclei and thalamus were found to be characterized by increases in grey matter volume.2-4 A recent review article 5 confirmed these results and concluded that structural alterations in patients with OCD are widespread and occur most probably at a network level, with cortical tissue reductions and a tendency toward increases in grey matter volume of subcortical limbic areas. These subcortical tissue increases were also corroborated by a recent meta/mega-analysis of the ENIGMA OCD imaging consortium. 6 Additionally, this meta/mega-analysis showed that the neuroplasticity of specific areas depends on the age of the studied sample (i.e., smaller hippocampal but larger pallidum volumes were prominent in adults with OCD, whereas only larger thalamic volumes were specific for pediatric patients). Besides grey matter volume alterations in patients with OCD, significantly decreased grey matter thickness in partly overlapping areas (i.e., limbic, parietal and temporal areas) was also found in another recent mega-analysis. 7 It is Background: Mounting evidence indicates the presence of structural brain alterations in individuals with obsessive-compulsive disorder (OCD). Findings are, however, rather heterogeneous, which may be partly because of differences in methodological approaches or clinical sample characteristics. The aim of the present study was to analyze the whole brain cortical volume, surface area and thickness in a large sample of patients with OCD compared with age-and sex-matched healthy controls. Methods: We conducted whole brain surfacebased analyses of grey matter measures using the automated FreeSurfer software in patients with OCD and matched controls. Group analyses were performed and corrected for multiple testing using Monte Carlo simulations (p < 0.05). Altered brain regions and their average morphological values were associated to symptom severity and type (Yale-Brown Obsessive Compulsive Scale scores). Results:We included 75 patients and 75 controls in our analyses. Patients with OCD showed decreases in both volume and surface area compared with healthy ...

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“…Tension-induced folding suggests that strongly interconnected regions pull towards each other and lead to the formation of gyri, whereas more sparsely connected fibers elongate to leave room for sulci 10 . The "grey matter hypothesis" suggests that gyrification may be the result of cell proliferation in the outer subventricular zone during early gestation 11 . This hypothesis is based on findings in transgenic mice, which showed increased cerebral cortical SA and human-like folds after controlling the cell cycle exit of neural precursors in the outer subventricular zone 12 .…”

Section: Introductionmentioning

confidence: 99%

Reduced Gyrification Is Related to Reduced Interhemispheric Connectivity in Autism Spectrum Disorders

Bos

Merchán-Naranjo

Martínez

et al. 2015

Journal of the American Academy of Child & Adolescent Psych

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Objective. Autism spectrum disorders (ASD) have been associated with atypical cortical grey and subcortical white matter development. Neurodevelopmental theories postulate that a relation between cortical maturation and structural brain connectivity may exist. We therefore investigated the development of gyrification and white matter connectivity and their relationship in individuals with ASD and their typically developing peers.Method. T1-and diffusion-weighted images were acquired from a representative sample of 30 children and adolescents with ASD (aged 8 to 18 years), and 29 typically developing children matched for age, sex, hand preference, and socioeconomic status. The FreeSurfer suite was used to calculate cortical volume, surface area, and gyrification index. Measures of structural connectivity were estimated using probabilistic tractography and tract-based spatial statistics (TBSS).Results. Left prefrontal and parietal cortex showed a relative, age-dependent decrease in gyrification index in children and adolescents with ASD compared to typically developing controls. This result was replicated in an age and IQ-matched sample provided by the Autism Brain Imaging Data Exchange (ABIDE) initiative. Furthermore, tractography and TBSS showed a complementary pattern, where left prefrontal gyrification was negatively related to radial diffusivity in the forceps minor in participants with ASD.Conclusion. The present study builds on earlier findings of abnormal gyrification and structural connectivity in the prefrontal cortex in ASD. It provides a more comprehensive neurodevelopmental characterization of ASD, involving interdependent changes in microstructural white and cortical grey matter. The findings of related abnormal patterns of gyrification and white matter connectivity support the notion of the intertwined development of two major morphometric domains in ASD.

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Development of cortical folding during evolution and ontogeny

Cited by 473 publications

References 88 publications

An Adaptive Threshold in Mammalian Neocortical Evolution

An Adaptive Threshold in Mammalian Neocortical Evolution

Structural alterations in patients with obsessive–compulsive disorder: a surface-based analysis of cortical volume, surface area and thickness

Reduced Gyrification Is Related to Reduced Interhemispheric Connectivity in Autism Spectrum Disorders

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