Brain development and aging: Overlapping and unique patterns of change
Center for the Study of Human Cognition, Department of Psychology, University of Oslo, Oslo, Norway. Electronic address: . NeuroImage
(Impact Factor: 6.36).
12/2012; 68. DOI: 10.1016/j.neuroimage.2012.11.039
Early-life development is characterized by dramatic changes, impacting lifespan function more than changes in any other period. Developmental origins of neurocognitive late-life functions are acknowledged, but detailed longitudinal magnetic resonance imaging studies of brain maturation and direct comparisons with aging are lacking. To these aims, a novel method was used to measure longitudinal volume changes in development (n=85, 8-22years) and aging (n=142, 60-91years). Developmental reductions exceeded 1% annually in much of cortex, more than double that seen in aging, with a posterior-to-anterior gradient. Cortical reductions were greater than subcortical during development, while the opposite held in aging. The pattern of lateral cortical changes was similar across development and aging, but the pronounced medial temporal reduction in aging was not precast in development. Converging patterns of change in adolescents and elderly, particularly in medial prefrontal areas, suggest that late developed cortices are especially vulnerable to atrophy in aging. A key question in future research will be to disentangle the neurobiological underpinnings for the differences and the similarities between brain changes in development and aging.
Available from: Francis Eustache
- "; Mills, Lalonde, Clasen, Giedd, & Blakemore, 2014; Pfeifer & Blakemore, 2012; Pfeifer & Peake, 2012; Sebastian et al., 2008). Longitudinal structural neuroimaging studies show that the mPFC is one of the latest developing regions (Mills, Goddings, Clasen, Giedd, & Blakemore, 2014; Mills, Lalonde et al., 2014; Tamnes et al., 2013). Developmental fMRI studies on metalizing (including self-reference processing studies described below) showed that mPFC activity increases between childhood and adolescence, followed by a decrease between adolescence and adulthood (Blakemore, 2008, 2012). "
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ABSTRACT: Adolescence is marked by the development of personal identity and is associated with structural and functional changes in brain regions associated with Self processing. Yet, little is known about the neural correlates of self-reference processing and self-reference effect in adolescents. This functional magnetic resonance imaging study consists of a self-reference paradigm followed by a recognition test proposed to 30 healthy adolescents aged 13–18 years old. Results showed that the rostral anterior cingulate cortex is specifically involved in self-reference processing and that this specialization develops gradually from 13 to 18 years old. The self-reference effect is associated with increased brain activation changes during encoding, suggesting that the beneficial effect of Self on memory may occur at encoding of self-referential information, rather than at retrieval.
Child Development 10/2015; DOI:10.1111/cdev.12440 · 4.92 Impact Factor
Available from: Catherine L Sebastian
- "Structural connections between these regions continue to mature during adolescence, resulting in greater top-down control, and strengthening pathways that are called upon routinely (Gee et al., 2013). This improved connectivity is largely a result of a linear increase in white matter volume and density in adolescence; however, this decelerates into adulthood (Giedd et al., 1999; Ostby et al., 2009; Tamnes et al., 2013). Developmental changes in white matter are thought to reflect ongoing axonal myelination, increasing the efficiency of neurotransmission between brain regions (although see Perrin et al., 2009, for a discussion on sex differences in the maturation of white matter; specifically they found age-related increases in axonal calibre in males and increased myelination in females, suggesting a more complex developmental picture). "
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ABSTRACT: Emotion regulation is the ability to recruit processes to influence emotion generation. In recent years there has been mounting interest in how emotions are regulated at behavioural and neural levels, as well as in the relevance of emotional dysregulation to psychopathology. During adolescence, brain regions involved in affect generation and regulation, including the limbic system and prefrontal cortex, undergo protracted structural and functional development. Adolescence is also a time of increasing vulnerability to internalising and externalising psychopathologies associated with poor emotion regulation, including depression, anxiety and antisocial behaviour. It is therefore of particular interest to understand how emotion regulation develops over this time, and how this relates to ongoing brain development. However, to date relatively little research has addressed these questions directly. This review will discuss existing research in these areas in both typical adolescence and in adolescent psychopathology, and will highlight opportunities for future research. In particular, it is important to consider the social context in which adolescent emotion regulation develops. It is possible that while adolescence may be a time of vulnerability to emotional dysregulation, scaffolding the development of emotion regulation during this time may be a fruitful preventative target for psychopathology.
Copyright © 2015 The Authors. Published by Elsevier Ltd.. All rights reserved.
Developmental Cognitive Neuroscience 07/2015; DOI:10.1016/j.dcn.2015.07.006 · 3.83 Impact Factor
Available from: Torgeir Moberget
- "Notably, the developing cerebral cortex shows an initial growth in early childhood (Lyall et al., in press), followed by a subsequent decrease. This inverted U-shape is evident in both grey matter density and grey matter volume (Taki et al., 2013), cortical thickness (Lyall et al., in press; Shaw et al., 2008; Tamnes et al., 2013) and surface area (Fjell et al., 2015; Wierenga et al., 2014) measures, with different peak ages for these respective measures ranging from about 2 years for cortical thickness (Lyall et al., in press) to about 8–12 years for cortical surface area (Brown et al., 2012; Wierenga et al., 2014). While the mechanisms underlying these developmental trajectories remain unclear, they likely involve at least an initial increase in the number of neurons and synapses per neuron, and a subsequent decrease in the number of synapses as well as an increase of cortical myelination during adolescence and young adulthood (Taki et al., 2013). "
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ABSTRACT: The cerebellum is connected to extensive regions of the cerebrum, and cognitive deficits following cerebellar lesions may thus be related to disrupted cerebello-cerebral connectivity. Moreover, early cerebellar lesions could affect distal brain development, effectively inducing long-term changes in brain structure and cognitive function. Here, we characterize supratentorial brain structure and cognitive function in 20 adult patients treated for cerebellar tumours in childhood (mean age at surgery: 7.1 years) and 26 matched controls. Relative to controls, patients showed reduced cognitive function and increased grey matter density in bilateral cingulum, left orbitofrontal cortex and the left hippocampus. Within the patient group, increased grey matter density in these regions was associated with decreased performance on tests of processing speed and executive function. Further, diffusion tensor imaging revealed widespread alterations in white matter microstructure in patients. While current ventricle volume (an index of previous hydrocephalus severity it patients) was associated with grey matter density and white matter microstructure in patients, this could only partially account for the observed group differences in brain structure and cognitive function. In conclusion, our results show distal effects of cerebellar lesions on cerebral integrity and wiring, likely caused by a combination of neurodegenerative processes and perturbed neurodevelopment.
Neuropsychologia 02/2015; 69:218-231. DOI:10.1016/j.neuropsychologia.2015.02.007 · 3.30 Impact Factor
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