Biology subjects

Fjell, A. M.

Publications and source records attributed to Fjell, A. M..

36 records · Page 2Linked to original sources

bioRxiv2021

Brain age relates to early life factors but not to accelerated brain aging

Brain age is a widely used index for quantifying individuals brain health as deviation from a normative brain aging trajectory. Higher than expected brain age is thought partially to reflect above-average rate of brain aging. We explicitly tested this assumption in two large datasets and found no association between cross-sectional brain age and steeper brain decline measured longitudinally. Rather, brain age in adulthood was associated with early-life influences indexed by birth weight and polygenic scores. The results call for nuanced interpretations of cross-sectional indices of the aging brain and question their validity as markers of ongoing within-person changes of the aging brain. Longitudinal imaging data should be preferred whenever the goal is to understand individual change trajectories of brain and cognition in aging.

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bioRxiv2020

Reliability and sensitivity of two whole-brain segmentation approaches included in FreeSurfer - ASEG and SAMSEG

An accurate and reliable whole-brain segmentation is a key aspect of longitudinal neuroimaging studies. The ability to measure structural changes reliably is fundamental to detect confidently biological effects, especially when these affects are small. In this work, we undertake a thorough comparative analysis of reliability, bias, sensitivity to detect longitudinal change and diagnostic sensitivity to Alzheimers disease of two subcortical segmentation methods, Automatic Segmentation (ASEG) and Sequence Adaptive Multimodal Segmentation (SAMSEG). These are provided by the recently released version 7.1 of the open-source neuroimaging package FreeSurfer, with ASEG being the default segmentation method. First, we use a large sample of participants (n = 1629) distributed across the lifespan (age range = 4-93 years) to assess the within-session test-retest reliability in eight bilateral subcortical structures: amygdala, caudate, hippocampus, lateral ventricles, nucleus accumbens, pallidum, putamen and thalamus. We performed the analyses separately for a sub-sample scanned on a 1.5T Siemens Avanto (n = 774) and a sub-sample scanned on a 3T Siemens Skyra (n = 855). The absolute symmetrized percent differences across the lifespan indicated relatively constant reliability trajectories across age except for the younger children in the Avanto dataset for ASEG. Although both methods showed high reliability (ICC > 0.95), SAMSEG yielded significantly lower volumetric differences between repeated measures for all subcortical segmentations (p < 0.05) and higher spatial overlap in all structures except putamen, which had significantly higher spatial overlap for ASEG. Second, we tested how well each method was able to detect neuroanatomic volumetric change using longitudinal follow up scans (n = 491 for Avanto and n = 245 for Skyra; interscan interval = 1-10 years). Both methods showed excellent ability to detect longitudinal change, but yielded age-trajectories with notable differences for most structures, including the hippocampus and the amygdala. For instance, ASEG hippocampal volumes showed a steady age-decline from subjects in their twenties, while SAMSEG hippocampal volumes were stable until their sixties. Finally, we tested sensitivity of each method to clinically relevant change. We compared annual rate of hippocampal atrophy in a group of cognitively normal older adults (n = 20), patients with mild cognitive impairment (n = 20) and patients with Alzheimers disease (n = 20). SAMSEG was more sensitive to detect differences in atrophy between the groups, demonstrating ability to detect clinically relevant longitudinal changes. Both ASEG and SAMSEG were reliable and led to detection of within-person longitudinal change. However, SAMSEG yielded more consistent measurements between repeated scans without a lack of sensitivity to changes.

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bioRxiv2020

Development of attention networks from childhood to young adulthood: A study of performance, intraindividual variability and cortical thickness

Human cognitive development is manifold, with different functions developing at different speeds at different ages. Attention is an important domain of this cognitive development, and involves distinct developmental trajectories in separate functions, including conflict processing, selection of sensory input and alertness. In children, several studies using the Attention Network Test (ANT) have investigated the development of three attentional networks that carry out the functions of executive control, orienting and alerting. There is, however, a lack of studies on the development of these attentional components across adolescence, limiting our understanding of their protracted development. To fill this knowledge gap, we performed a mixed cross-sectional and longitudinal study using mixed methods to examine the development of the attentional components and their intraindividual variability from late childhood to young adulthood (n = 287, n observations = 408, age range = 8.5-26.7 years, mean follow up interval = 4.4 years). The results indicated that executive control stabilized during late adolescence, while orienting and alerting continued to develop into young adulthood. In addition, a continuous development into young adulthood was observed for the intraindividual variability measures of orienting and alerting. In a subsample with available magnetic resonance imaging (MRI) data (n =169, n observations = 281), higher alerting scores were associated with thicker cortices within a right prefrontal cortical region and greater age-related cortical thinning in left rolandic operculum, while higher orienting scores were associated with greater age-related cortical thinning in frontal and parietal regions. Finally, increased consistency of orienting performance was associated with thinner cortex in prefrontal regions and reduced age-related thinning in frontal regions.

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bioRxiv2020

Comparative morphology of the corpus callosum across the adult lifespan in chimpanzees (Pan troglodytes) and humans

The human corpus callosum exhibits substantial atrophy in old age, which is stronger than what would be predicted from parallel changes in overall brain anatomy. To date, however, it has not been conclusively established whether this accentuated decline represents a common feature of brain aging across species, or whether it is a specific characteristic of the aging human brain. In the present cross-sectional study, we address this question by comparing age-related difference in corpus callosum morphology of chimpanzees and humans. For this purpose, we measured total midsagittal area and regional thickness of the corpus callosum from T1-weighted MRI data from 213 chimpanzees, aged between 9 and 54 years. The results were compared with data drawn from a large-scale human samples which was age-range matched using two strategies: (a) matching by chronological age (human sample size: n = 562), or (b) matching by accounting for differences in longevity and various maturational events between the species (i.e., adjusted human age range: 13.6 to 80.9 years; n = 664). Using generalized additive modelling to fit and compare aging trajectories, we found significant differences between the two species. The chimpanzee aging trajectory compared to the human trajectory was characterized by a slower increase from adolescence to middle adulthood, and by a lack of substantial decline from middle to old adulthood, which, however, was present in humans. Thus, the accentuated decline of the corpus callosum found in aging humans, is not an universal characteristic of the aging brain, and appears to be human-specific.

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bioRxiv2020

Asymmetric thinning of the cerebral cortex across the adult lifespan is accelerated in Alzheimer's Disease

Normal aging and Alzheimers Disease (AD) are accompanied by large-scale alterations in brain organization that undermine brain function. Although hemispheric asymmetry is a global organizing feature of cortex thought to promote brain efficiency, current descriptions of cortical thinning in aging and AD have largely overlooked cortical asymmetry. Consequently, the foundational question of whether and where the cerebral hemispheres change at different rates in aging and AD remains open. First, applying vertex-wise data-driven clustering in a longitudinal discovery sample (aged 20-89; 2577 observations; 1851 longitudinal) we identified cortical regions exhibiting similar age-trajectories of asymmetry across the adult lifespan. Next, we sought replication in 4 independent longitudinal aging cohorts. We show that higher-order regions of cortex that exhibit pronounced asymmetry at age ~20 also show asymmetry change in aging. Results revealed that both leftward and rightward asymmetry is progressively lost on a similar time-scale across adult life. Hence, faster thinning of the (previously) thicker homotopic hemisphere is a feature of aging. This simple organizational principle showed high consistency across multiple aging cohorts in the Lifebrain consortium, and both the topological patterns and temporal dynamics of asymmetry-loss were markedly similar across replicating samples. Finally, we show that regions exhibiting gradual asymmetry-loss over healthy adult life exhibit faster asymmetry-change in AD. Overall, our results suggest a system-wide breakdown in the adaptive asymmetric organization of cortex across adult life which is further accelerated in AD, and may implicate thickness asymmetry as a viable marker for declining hemispheric specialization in aging and AD. SignificanceThe brain becomes progressively disorganized with age, and brain alterations accelerated in Alzheimers disease may occur gradually over the lifespan. Although hemispheric asymmetry aids efficient network organization, efforts to identify structural markers of age-related decline have largely overlooked cortical asymmetry. Here we show the hemisphere that is thicker when younger, thins faster. This leads to progressive system-wide loss of regional thickness asymmetry across life. In multiple aging cohorts, asymmetry-loss showed high reproducibility topologically across cortex and similar timing-of-change in aging. Asymmetry-change was further accelerated in AD. Our findings uncover a new principle of brain aging - thicker homotopic cortex thins faster - and suggest we may have unveiled a structural marker for a widely-hypothesized decline in hemispheric specialization in aging and AD.

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bioRxiv2020

Electrophysiological and behavioral indices of cognitive conflict processing across adolescence

Cognitive control enables goal-oriented adaptation to a fast-changing environment and has a slow developmental trajectory that spans into young adulthood. The specifics of this development are still poorly understood, as are the neurodevelopmental mechanisms that drive it. In a cross-sectional sample of participants 8-19 years old (n = 108), we used blind source separation of EEG data recorded in a Flanker task to derive electrophysiological measures of attention and the processing of cognitive conflict, including a frontal negative component corresponding to the N2 and a parietal positive component corresponding to the P3. Additionally, we examined multiple behavioral measures of interference control derived from the Flanker, Stroop, and Anti-saccade tasks. We found a positive association between age and the amplitude of the parietal positive component, while there was no relationship between age and the amplitude of the frontal negative component. A stronger frontal negative amplitude was, however, age-independently related to better performance on both Stroop and Anti-saccade measures of interference control. Finally, we examined post-conflict behavioral adjustment on the Flanker task. A Gratton effect was found with slower reaction times on current congruent and better accuracy on current incongruent trials when preceded by incongruent as opposed to congruent trials. The Gratton effect on accuracy was positively associated with age. Together, the findings suggest a multifaceted developmental pattern in neurocognitive mechanisms for conflict processing across adolescence, with a more protracted development of the parietal positive compared to the frontal negative component.

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bioRxiv2020

Sleep Efficiency Relates to Hippocampal Integrity Decline in β-Amyloid Positive Adults

BackgroundTo test the hypothesis that worse self-reported sleep relates to memory decay and reduced hippocampal integrity as indexed by increased intra-hippocampal water diffusion, and that the relations are stronger in the presence of {beta}-amyloid (A{beta}) accumulation, a marker of Alzheimers disease (AD) pathology. MethodsTwo-hundred and forty-three cognitively healthy participants, aged 19-81 years, completed the Pittsburgh Sleep Quality Index, and 2 diffusion tensor imaging sessions, on average 3 years apart, allowing measures of decline in hippocampal microstructural integrity as indexed by increased mean diffusivity. We measured memory decay using delayed recall from the California Verbal Learning Test. 18F-Flutemetamol positron emission tomography, in 108 participants above 44 years of age, yielded 23 A{beta} positive. Genotyping enabled controlling for APOE {varepsilon}4 status, and polygenic scores for sleep efficiency and AD. ResultsWorse global sleep quality and sleep efficiency related to more rapid reduction in hippocampal microstructural integrity over time. Focusing on sleep efficiency, the relation was stronger in presence of A{beta} accumulation. Sleep efficiency related to memory decay indirectly via hippocampal integrity decline. The results were not explained by genetic risk for sleep efficiency and AD. ConclusionsPoor self-reported sleep efficiency related to decline in hippocampal integrity, especially in the presence of A{beta} accumulation. Poor sleep and hippocampal microstructural decline may partly explain memory decline in older adults with A{beta} pathology. The relationships were not explained by genetic risk. Poor self-reported sleep efficiency might constitute a risk factor for AD, although the causal mechanisms driving the of observed associations remain unknown.

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bioRxiv2020

The functional foundations of episodic memory remain stable throughout the lifespan

It is suggested that the functional mechanisms behind specific forms of cognition, particularly episodic memory, may be dynamic over the lifespan and that cognitive preservation or decay in older age thus relies on age-specific mechanisms such as compensatory processes. Here instead, we tested whether the functional foundations of successful episodic memory encoding adhere to a principle of lifespan continuity, shaped by developmental, structural and evolutionary influences. We identified the generic lifespan patterns of memory encoding function across the brain (n = 540; age range = 6 - 82 years). The lifespan trajectories of brain activity were organized in a topologically meaningful manner and aligned to fundamental aspects of brain organization, such as large-scale connectivity hierarchies and evolutionary cortical expansion gradients. None of the normative trajectories of encoding function was solely determined by late-life patterns of activity, but rather showed continuities across development and adulthood. Inter-individual differences in activity in age-sensitive regions were predicted by general cognitive abilities and variation in grey matter structure, which are core variables of cognitive and structural change throughout the lifespan. Altogether, the results provide evidence for the lifelong continuity of the functional foundations of episodic memory which are bounded by both brain architecture and core mechanisms of cognitive and structural change over life. We provide novel support for a perspective on memory aging in which maintenance and decay of episodic memory in older age needs to be understood from a comprehensive life-long perspective rather than as a late-life phenomenon only. Significance statementIt is suggested that cognitive function in older age largely relies on late-life specific mechanisms such as compensatory processes. In contrast, here we tested whether and to what degree brain activity during episodic memory encoding adheres to fundamental principles of life-long brain organization and continuity. The results revealed that generic lifespan trajectories of memory encoding function were not specific to late-life. Instead, the age-trajectories showed a continuity through life, were related to fundamental features of brain structure and cognition and to functional and evolutionary hierarchies. We argue that rather than focusing on older-age specific mechanisms, a framework that takes lifespan mechanisms of cognition and brain anatomy into account is necessary to understand episodic memory vulnerability in older age.

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bioRxiv2019

Self-reported sleep relates to hippocampal atrophy across the adult lifespan - results from the Lifebrain consortium

BackgroundPoor sleep is associated with multiple age-related neurodegenerative and neuropsychiatric conditions. The hippocampus plays a special role in sleep and sleep-dependent cognition, and accelerated hippocampal atrophy is typically seen with higher age. Hence, it is critical to establish how the relationship between sleep and hippocampal volume loss unfolds across the adult lifespan.\n\nMethodsSelf-reported sleep measures and MRI-derived hippocampal volumes were obtained from 3105 cognitively normal participants (18-90 years) from major European brain studies in the Lifebrain consortium. Hippocampal volume change was estimated from 5116 MRIs from 1299 participants, covering up to 11 years. Cross-sectional analyses were repeated in a sample of 21390 participants from the UK Biobank.\n\nResultsThe relationship between self-reported sleep and age differed across sleep items. Sleep duration, efficiency, problems, and use of medication worsened monotonously with age, whereas subjective sleep quality, sleep latency, and daytime tiredness improved. Women reported worse sleep in general than men, but the relationship to age was similar. No cross-sectional sleep - hippocampal volume relationships was found. However, worse sleep quality, efficiency, problems, and daytime tiredness were related to greater hippocampal volume loss over time, with high scorers showing on average 0.22% greater annual loss than low scorers. Simulations showed that longitudinal effects were too small to be detected as age-interactions in cross-sectional analyses.\n\nConclusionsWorse self-reported sleep is associated with higher rates of hippocampal decline across the adult lifespan. This suggests that sleep is relevant to understand individual differences in hippocampal atrophy, but limited effect sizes call for cautious interpretation.

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bioRxiv2019

Genetic risk for Alzheimer`s disease predicts hippocampal volume through the lifespan

INTRODUCTIONIt is unknown whether genetic risk for Alzheimers disease (AD) represents a stable influence on the brain from early in life, or whether effects are age-dependent. It is critical to characterize the effects of genetic risk factors on the primary neural substrate of AD, the hippocampus, throughout life.\n\nMETHODSRelations of polygenic risk score (PGS) for AD, including variants in Apolipoprotein E (APOE) with hippocampal volume and its change were assessed in a healthy longitudinal lifespan sample (n = 1181, 4-95 years), followed for up to 11 years with a total of 2690 MRI scans.\n\nRESULTSAD-PGS showed a significant negative effect on hippocampal volume. Offset effects of AD-PGS and APOE {varepsilon}4 were present in hippocampal development, and interactions between age and genetic risk on volume change were not consistently observed. DISCUSSION: Endophenotypic manifestation of polygenic risk for AD may be seen across the lifespan in healthy persons.\n\nHighlightsO_LIGenetic risk for AD affects the hippocampus throughout the lifespan\nC_LIO_LIAPOE {varepsilon}4 carriers have smaller hippocampi in development\nC_LIO_LIDifferent effects of genetic risk at different ages were not consistently observed\nC_LIO_LIGenetic factors increasing risk for AD impact healthy persons throughout life\nC_LIO_LIA broader population and age range are relevant targets for attempts to prevent AD\nC_LI

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bioRxiv2019

Cellular correlates of cortical thinning throughout the lifespan

Cortical thinning occurs throughout the entire life and extends to late-life neurodegeneration, yet the neurobiological substrates are poorly understood. Here, we used a virtual-histology technique and gene expression data from the Allen Human Brain Atlas to compare the regional profiles of longitudinal cortical thinning through life (4004 MRIs) with those of gene expression for several neuronal and non-neuronal cell types. The results were replicated in three independent longitudinal datasets. We found that inter-regional profiles of cortical thinning related to expression profiles for marker genes of CA1 pyramidal cells, astrocytes and microglia during development and in aging. During the two stages of life, the relationships went in opposite directions: greater gene expression related to less thinning in development and vice versa in aging. The association between cortical thinning and cell-specific gene expression was also present in mild cognitive impairment and Alzheimers Disease. These findings suggest a role of astrocytes and microglia in promoting and supporting neuronal growth and dendritic structures through life that affects cortical thickness during development, aging, and neurodegeneration. Overall, the findings contribute to our understanding of the neurobiology underlying variations in MRI-derived estimates of cortical thinning through life and late-life disease.

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bioRxiv2019

Lifespan trajectories and relationships to memory of the macro- and microstructure of the anterior and posterior hippocampus - a longitudinal multi-modal imaging study

There is evidence for a hippocampal long axis anterior-posterior (AP) differentiation in memory processing, which may have implications for the changes in episodic memory performance typically seen across development and aging. The hippocampal formation shows substantial structural changes with age, but the lifespan trajectories of hippocampal sub-regions along the AP axis are not established. The aim of the present study was to test whether the micro- and macro-structural age-trajectories of the anterior (aHC) and posterior (pHC) hippocampus are different. In a single-center longitudinal study, 1790 cognitively healthy participants, 4.1-93.4 years of age, underwent a total of 3367 MRI examinations and 3033 memory tests sessions over 1-6 time points, spanning an interval up to 11.1 years. T1-weighted scans were used to estimate the volume of aHC and pHC, and diffusion tensor imaging to measure mean diffusion (MD) within each region. We found that the macro- and microstructural lifespan-trajectories of aHC and pHC were clearly distinguishable, with partly common and partly unique variance shared with age. aHC showed a protracted period of microstructural development, while pHC microstructural development as indexed by MD was more or less completed in early childhood. In contrast, pHC showed larger unique aging-related changes. A similar aHC - pHC difference was observed for volume, although not as evident as for microstructure. All sub-regions showed age-dependent relationships to episodic memory function. For aHC micro- and macrostructure, the relationships to verbal memory performance varied significantly with age, being stronger among the older participants. Future research should disentangle the relationship between these structural properties and different memory processes - encoding vs. retrieval in particular - across the lifespan.

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bioRxiv2018

Error processing in the adolescent brain: Age-related differences in electrophysiology and links with post-error adjustments but no relationship to cingulate cortex structure

Detecting errors and adjusting behaviour appropriately are fundamental cognitive abilities that are known to improve through adolescence. The underlying mechanisms of this development, however, are still poorly understood. To address this knowledge gap, we performed a thorough investigation of error processing in a Flanker task in a cross-sectional sample of participants 8 to 19 years of age (n = 98). We examined age-differences in event related potentials known to be associated with error processing, namely the error-related negativity (ERN) and the error positivity (Pe), as well as their relationships with task performance, post-error adjustments and regional cingulate cortex thickness and surface area. We found that ERN amplitude increased with age, while Pe amplitude remained constant. A more negative ERN was associated with higher task accuracy and faster reaction times, while a more positive Pe was associated with higher accuracy, independently of age. When estimating post-error adjustments from trials following both incongruent and congruent trials, post-error slowing and post-error improvement in accuracy both increased with age, but this was only found for post-error slowing when only analysing trials following incongruent trials. There were no age-independent associations between either ERN or Pe amplitude and cingulate cortex thickness or area measures.

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bioRxiv2018

Age-differences in functional asymmetry during memory retrieval revisited: no evidence for contralateral over-activation or compensation

Brain asymmetry is inherent to cognitive processing and seems to reflect processing efficiency. Lower frontal asymmetry is often observed in older adults during memory retrieval, yet it is unclear whether lower asymmetry implies an age-related increase in contralateral recruitment, whether less asymmetry reflects compensation, is limited to frontal regions, or predicts neurocognitive stability or decline. We assessed age-differences in asymmetry across the entire cerebral cortex, using fMRI data from 89 young and 76 older adults during successful retrieval, and surface-based methods that allowed direct homotopic comparison of activity between hemispheres. An extensive left-asymmetric network facilitated retrieval in both young and older adults, whereas diverse frontal and parietal regions exhibited lower asymmetry in older adults. However, lower asymmetry was not associated with age-related increases in contralateral recruitment, but primarily reflected either less deactivation in contralateral regions reliably signalling retrieval failure in the young, or lower recruitment of the dominant hemisphere--suggesting that functional deficits may drive lower asymmetry in older brains, not compensatory activity. Lower asymmetry neither predicted current memory performance, nor the extent of memory change across the preceding [~]8 years in older adults. Together, these findings are inconsistent with a compensation account for lower asymmetry during retrieval and aging.

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bioRxiv2018

The hotspots in primate cortical brain evolution support supramodal cognitive flexibility

Primate cortical evolution has been characterized by massive and disproportionate expansion of a set of specific regions in the neocortex. The associated increase in neocortical neurons comes with a high metabolic cost, thus the functions served by these regions must have conferred significant evolutionary advantage. Here, across a series of experiments, we show that the evolutionary high-expanding hotspots - as estimated from patterns of evolutionary expansion from several primate species - share functional connections with different brain networks in a context-dependent manner. This capacity of the hotspots to connect flexibly with various specialized brain networks depending on particular cognitive requirements suggests that their selective growth and sustainment in evolution has been linked to their involvement in supramodal cognition. In accordance with an evolutionary-developmental view, we find that this ability to flexibly modulate functional connections as a function of cognitive state emerges gradually through childhood, with a prolonged developmental trajectory plateauing in young adulthood.

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bioRxiv2018

Development and decline of the hippocampal long-axis specialization and differentiation during encoding and retrieval of episodic memories

Change in hippocampal function is a major factor in lifespan development and decline of episodic memory. Evidence indicates a long-axis specialization where anterior hippocampus is more engaged during encoding and posterior during retrieval. We tested the lifespan trajectory of hippocampal long-axis episodic memory-related activity and functional connectivity (FC). 496 participants (6.8-80.8 years) were scanned with functional MRI while encoding and retrieving associative memories. We found clear evidence for a long-axis encoding-retrieval specialization. These long-axis effects declined linearly during development and aging, eventually vanishing in the older adults. This was mainly driven by age effects on retrieval. Retrieval was associated with gradually lower activity from childhood to adulthood, followed by positive age-relationships until 70 years. Interestingly, this pattern characterized task engagement regardless of memory success or failure. Children engaged posterior hippocampus more than anterior, while anterior hippocampus was more activated relative to posterior already in teenagers. Intra-hippocampal connectivity increased during task, and this increase declined with age. In sum, the results suggest that hippocampal long-axis differentiation and communication during episodic memory tasks develop rapidly during childhood and adolescence, are markedly different in older compared to younger adults, and are related to task engagement, not the successful completion of the task.

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bioRxiv2018

Waves of maturation and senescence in micro-structural MRI markers of human cortical myelination over the lifespan

Seminal human brain histology work has demonstrated developmental waves of myelination. Here, using a micro-structural magnetic resonance imaging (MRI) marker linked to myelin, we studied fine-grained age differences to deduce waves of growth, stability, and decline of cortical myelination over the life-cycle. In 484 participants, aged 8-85 years, we fitted smooth growth curves to T1- to T2-weighted ratio in each of 360 regions from one of 7 cytoarchitectonic classes. From the first derivatives of these generally inverted-U trajectories, we defined three milestones: the age at peak growth; the age at onset of a stable plateau; and the age at the onset of decline. Age at peak growth had a bimodal distribution comprising an early (pre-pubertal) wave of primary sensory and motor cortices and a later (post-pubertal) wave of association, insular and limbic cortices. Most regions reached stability in the 30s but there was a second wave reaching stability in the 50s. Age at onset of decline was also bimodal: in some right hemisphere regions, the curve declined from the 60s, but in other left hemisphere regions, there was no significant decline from the stable plateau. These results are consistent with regionally heterogeneous waves of intracortical myelinogenesis and age-related demyelination.

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bioRxiv2018

Development of the P300 from childhood to adulthood: a multimodal EEG and MRI study

Maturation of attentional processes is central to cognitive development. The electrophysiological P300 is associated with rapid allocation of attention, and bridges stimulus and response processing. P300 is among the most studied and robust electrophysiological components, but how different subcomponents of the P300 develop from childhood to adulthood and relate to structural properties of the cerebral cortex is not well understood. We investigated age-related differences in both early visual and P300 components, and how individual differences in these components related to cortical structure in a cross-sectional sample of participants 8-19 years (n=86). Participants completed a three-stimulus visual oddball task while high-density EEG was recorded. Cortical surface area and thickness were estimated from T1-weighthed MRI. Group-level blind source separation of the EEG data identified two P300-like components, a fronto-central P300 and a parietal P300, as well as a component reflecting N1 and P2. Differences in activity across age were found for the parietal P300, N1 and P2, with the parietal P300 showing stronger activity for older participants, while N1 and P2 were stronger for younger participants. Stronger P300 components were positively associated with task performance, independently of age, while negative associations were found for P2 strength. Parietal P300 strength was age-independently associated with larger surface area in a region in left lateral inferior temporal cortex. We suggest that the age differences in component strength reflect development of attentional mechanisms, with increased brain responses to task-relevant stimuli representing an increasing ability to focus on relevant information and to respond accurately and efficiently.

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