Critical Periods in Brain Development

Smart, James L.

doi:10.1002/9780470514047.ch8

Cited by 19 publications

(16 citation statements)

References 25 publications

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“…Studies on cognitive development have already noted links between the schedule of brain development and the pattern of maternal care. For example, behavioral imprinting in birds and mammals can only occur after hatching or birth, respectively [101]. However, species might differ substantially as to whether adaptation in critical windows occurred through genetic versus non-genetic mechanisms, making it difficult to interpret results in the context of human physiology.…”

Section: Opportunities To Test the Hypothesismentioning

confidence: 99%

Adaptive variability in the duration of critical windows of plasticity: Implications for the programming of obesity

Wells¹

2014

Evolution, Medicine, and Public Health

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Developmental plasticity underlies widespread associations between early-life exposures and many components of adult phenotype, including the risk of chronic diseases. Humans take almost two decades to reach reproductive maturity, and yet the ‘critical windows’ of physiological sensitivity that confer developmental plasticity tend to close during fetal life or infancy. While several explanations for lengthy human maturation have been offered, the brevity of physiological plasticity has received less attention. I argue that offspring plasticity is only viable within the niche of maternal care, and that as this protection is withdrawn, the offspring is obliged to canalize many developmental traits in order to minimize environmental disruptions. The schedule of maternal care may therefore shape the duration of critical windows, and since the duration of this care is subject to parent–offspring conflict, the resolution of this conflict may shape the duration of critical windows. This perspective may help understand (i) why windows close at different times for different traits, and (ii) why the duration of critical windows may vary across human populations. The issue is explored in relation to population differences in the association between infant weight gain and later body composition. The occupation of more stable environments by western populations may have favoured earlier closure of the critical window during which growth in lean mass is sensitive to nutritional intake. This may paradoxically have elevated the risk of obesity following rapid infant weight gain in such populations.

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Section: Opportunities To Test the Hypothesismentioning

confidence: 99%

Adaptive variability in the duration of critical windows of plasticity: Implications for the programming of obesity

Wells¹

2014

Evolution, Medicine, and Public Health

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“…Many studies now show clearly that specific nutritional deficits at critical stages of development limit fundamental components of growth that have long-lasting influences. Smart [13, 14] showed years ago that undernutrition of rat fetuses reduced brain growth overall as well as neuronal number and synapses, leading to later life reductions in brain size, cognitive capacity, and specific behaviors, such as learning. More recently, several groups have shown that brain growth of preterm infants is less than that of normally grown infants born at term, that this reduced brain growth is associated with cognitive delays, and that nutrition of the preterm infant with enriched diets (supplemented milk or preterm formulas, both with more protein) leads to larger brains and improved cognitive function, even into adolescence [15–17].…”

Section: Consequences Of Not Meeting the Goal Of Normal Fetal Growth mentioning

confidence: 99%

Strategies for Feeding the Preterm Infant

Hay¹

2008

Neonatology

189

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According to many experts in neonatal nutrition, the goal for nutrition of the preterm infant should be to achieve a postnatal growth rate approximating that of the normal fetus of the same gestational age. Unfortunately, most preterm infants, especially those born very preterm with extremely low birth weight, are not fed sufficient amounts of nutrients to produce normal fetal rates of growth and, as a result, end up growth-restricted during their hospital period after birth. Growth restriction is a significant problem, as numerous studies have shown definitively that undernutrition, especially of protein, at critical stages of development produces long-term short stature, organ growth failure, and both neuronal deficits of number and dendritic connections as well as later behavioral and cognitive outcomes. Furthermore, clinical follow-up studies have shown that among infants fed formulas, the nutrient content of the formula is directly and positively related to mental and motor outcomes later in life. Nutritional requirements do not stop at birth. Thus, delaying nutrition after birth ‘until the infant is stable’ ignores the fundamental point that without nutrition starting immediately after birth, the infant enters a catabolic condition, and catabolism does not contribute to normal development and growth. Oxygen is necessary for all metabolic processes. Recent trends to limit oxygen supply to prevent oxygen toxicity have the potential, particularly when the blood hemoglobin concentration falls to less than 8 g/dl, to develop growth failure. Glucose should be provided at 6–8 mg/min/kg as soon after birth as possible and adjusted according to frequent measurements of plasma glucose to achieve and maintain concentrations >45 mg/dl but <120 mg/dl to avoid the frequent problems of hyperglycemia and hypoglycemia. Similarly, lipid is required to provide at least 0.5 g/kg/day to prevent essential fatty acid deficiency. However, the high rate of carbohydrate and lipid supply that preterm infants often get, based on the incomplete assumption that this is necessary to promote protein growth, tends to produce increased fat in organs like the liver and heart as well as adipose tissue. More and better essential fatty acid nutrition is valuable, but more organ and adipose fat has no known benefit and many problems. Amino acids and protein are essential not only for body growth but for metabolic signaling, protein synthesis, and protein accretion. 3.5–4.0 g/kg/day are necessary to produce normal protein balance and growth in very preterm infants. Attempts to promote protein growth with insulin has many problems – it is ineffective while contributing to even further organ and adipose tissue fat deposition. Enteral feeding always is indicated and to date nearly all studies have shown that minimal enteral feeding approaches (e.g., ‘trophic feeds’) promote the capacity to feed enterally. Milk has distinct advantages over formulas in avoiding necrotizing enterocolitis (NEC), and while feeding is associated with NEC, minimal enteral ...

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“…In the past several decades, studies in rodents have provided substantial information on brain development [61][62][63][64][65][66]. Although there are variations in the rates of brain growth among mammals, comparisons of brain development between species are possible [66,67].…”

Section: Susceptibility Of the Developing Brain To Environmental Agentsmentioning

confidence: 99%

Antiepileptic drugs and the developing brain

Kaindl

Asimiadou

Manthey

et al. 2006

Cell. Mol. Life Sci.

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Epilepsy is the most common neurological disorder in young humans. Antiepileptic drugs (AEDs) which are used to treat seizures in infants, children and pregnant women can cause cognitive impairment, microcephaly and birth defects. Ion channels, neurotransmitters and second messenger systems constitute molecular targets of AEDs. The same targets regulate brain processes essential both for propagation of seizures and for learning, memory and emotional behavior. Thus, AEDs can influence brain function and brain development in undesired ways. Here we review mechanisms of action of AEDs, examine clinical evidence for their adverse effects in the developing human brain, and present studies on cognitive and behavioral effects in animal models. Furthermore, we discuss mechanisms responsible for adverse effects of AEDs in the developing mammalian brain, including interference with cell proliferation and migration, axonal arborization, synaptogenesis, synaptic plasticity and physiological apoptotic cell death.

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Critical Periods in Brain Development

Cited by 19 publications

References 25 publications

Adaptive variability in the duration of critical windows of plasticity: Implications for the programming of obesity

Adaptive variability in the duration of critical windows of plasticity: Implications for the programming of obesity

Strategies for Feeding the Preterm Infant

Antiepileptic drugs and the developing brain

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