Infant Development

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Infant environment (environmental factors that can affect the child's development)

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A brain imaging study of 162 healthy babies (2-25 months) has found that those who carried the ApoE4 gene (60 of the 162) tended to have increased brain growth in areas in the frontal lobe, and decreased growth in several areas in the middle and rear of the brain (precuneus, posterior/middle cingulate, lateral temporal, and medial occipitotemporal regions) — areas that tend to be affected in Alzheimer’s disease.

While this does not mean that those children are destined to develop Alzheimer’s, the findings do suggest brains of ApoE4 carriers tend to develop differently from those of non-carriers, and perhaps these early changes provide a “foothold” for the development of Alzheimer’s pathologies.

http://www.futurity.org/irregular-brain-growth-babies-risk-alzheimers/

[3567] Dean DC, Jerskey BA, Chen K, et al. Brain differences in infants at differential genetic risk for late-onset alzheimer disease: A cross-sectional imaging study. JAMA Neurology [Internet]. 2014 ;71(1):11 - 22. Available from: http://dx.doi.org/10.1001/jamaneurol.2013.4544

More than 10% of all babies are born preterm every year, and prematurity is a well-established risk factor for cognitive impairment at some level.

Prematurity affects working memory in particular

In a recent German study involving 1326 8-year-old children, it was found that being born preterm specifically affected the ability to solve tasks with a high cognitive load (i.e. greater demands on working memory), whereas tasks with a low load were largely unaffected.

These findings are consistent with other research suggesting that prematurity is associated in particular with difficulties in math, in complex problem-solving, and in simultaneous processing (such as occurs in recognition of spatial patterns).

There was also a clear dividing line, with deficits disproportionally higher for children born before the 34th week of pregnancy compared with children born after week 33.

Rate of cognitive impairment in premature infants

A Swedish study of 491 toddlers (2 ½ years) who had been born extremely preterm (less than 27 gestational weeks) found that 42% of them had no disability (compared with 78% of controls), 31% had mild disability, 16% had moderate disability, and 11% had severe disability. Unsurprisingly, there was an increase in moderate or severe disabilities with greater prematurity. There was no gender difference.

Cognitive impairment in premies linked to smaller brain tissue in specific regions

Why are some individuals affected by prematurity, why others aren’t? An analysis of brain imaging data of 97 adolescents who had very low birth weights, and whose academic progress has been followed, found that more than half of the babies that weighed less than 1.66 pounds and more than 30% of those less than 3.31 pounds at birth later had academic deficits. Academic deficits were linked to smaller brain volumes, and in particular to reduced volume of the caudate and corpus callosum, which are involved in connectivity, executive attention and motor control.

J. Jäkel, N. Baumann, D. Wolke (2013): Effects of gestational age at birth on cognitive performance: a function of cognitive workload demands, PLOS ONE, http://dx.plos.org/10.1371/journal.pone.0065219

[3444] Serenius F KK. Neurodevelopmental outcome in extremely preterm infants at 2.5 years after active perinatal care in sweden. JAMA [Internet]. 2013 ;309(17):1810 - 1820. Available from: http://dx.doi.org/10.1001/jama.2013.3786

[3442] Clark, C A, Fang H, Espy KA, Filipek PA, Juranek J, Bangert B, Hack M, Gerry H. Relation of neural structure to persistently low academic achievement: A longitudinal study of children with differing birth weights. Neuropsychology. 2013 ;27(3):364 - 377.

http://www.eurekalert.org/pub_releases/2013-05/rb-pba052713.php (1st study)

http://www.eurekalert.org/pub_releases/2013-04/tjnj-sen042513.php (2nd study)

http://www.eurekalert.org/pub_releases/2013-06/uoo-rbv061013.php (3rd study)

In the first study to analyze parent praise in a real-world setting, it’s been found that the kind of praise parents give their babies and toddlers influences the child’s motivation later on, and plays a role in children’s beliefs about themselves and their desire to take on challenges five years later.

The study analyzed video of 53 mothers interacting with their children at 1, 2, and 3 years of age. The children were interviewed about their attitudes five years later. Those who had received more praise directed at their actions and efforts were more likely to prefer challenges than those who heard praise directed at them personally (e.g., ‘You’re great, you’re amazing vs ‘Well done, you worked hard on that’). They were also more likely to believe that abilities and behavior could change and develop.

The amount of praise wasn’t important; what mattered was the ratio of ‘process praise’ compared to person praise.

Parents of boys tended to give more process praise than parents of girls.

http://www.futurity.org/society-culture/good-job-preps-kids-to-tackle-challenges/

[3317] Gunderson EA, Gripshover SJ, Romero C, Dweck CS, Goldin-Meadow S, Levine SC. Parent Praise to 1- to 3-Year-Olds Predicts Children's Motivational Frameworks 5 Years Later. Child Development [Internet]. 2013 :n/a - n/a. Available from: http://onlinelibrary.wiley.com/doi/10.1111/cdev.12064/abstract

In the light of a general increase in caesarean sections, it’s somewhat alarming to read about a mouse study that found that vaginal birth triggers the expression of a protein in the brains of newborns that improves brain development, and this protein expression is impaired in the brains of those delivered by C-section.

The protein in question —mitochondrial uncoupling protein 2 (UCP2) — is important for the development of neurons and circuits in the hippocampus. Indeed, it has a wide role, being involved in regulation of fuel utilization, mitochondrial bioenergetics, cell proliferation, neuroprotection and synaptogenesis. UCP2 is induced by cellular stress.

Among the mice, natural birth triggered UCP2 expression in the hippocampus (presumably because of the stress of the birth), which was reduced in those who were born by C-section. Not only were levels of UCP2 lower in C-section newborns, they continued to be lower through to adulthood.

Cell cultures revealed that inhibiting UCP2 led to decreased number of neurons, neuron size, number of dendrites, and number of presynaptic clusters. Mice with (chemically or genetically) inhibited UCP2 also showed behavioral differences indicative of greater levels of anxiety. They explored less, and they showed poorer spatial memory.

The effects of reduced UCP2 on neural growth means that factors that encourage the growth of new synapses, such as physical exercise, are likely to be much less useful (if useful at all). Could this explain why exercise seems to have no cognitive benefits for a small minority? (I’m speculating here.)

Although the researchers don’t touch on this (naturally enough, since this was a laboratory study), I would also speculate that, if the crucial factor is stress during the birth, this finding applies only to planned C-sections, not to those which become necessary during the course of labor.

UCP2 is also a critical factor in fatty acid utilization, which has a flow-on effect for the creation of new synapses. One important characteristic of breast milk is its high content of long chain fatty acids. It’s suggested that the triggering of UCP2 by natural birth may help the transition to breastfeeding. This in turn has its own benefits for brain development.

Grasp of fractions and long division predicts later math success

One possible approach to improving mathematics achievement comes from a recent study finding that fifth graders' understanding of fractions and division predicted high school students' knowledge of algebra and overall math achievement, even after statistically controlling for parents' education and income and for the children's own age, gender, I.Q., reading comprehension, working memory, and knowledge of whole number addition, subtraction and multiplication.

The study compared two nationally representative data sets, one from the U.S. and one from the United Kingdom. The U.S. set included 599 children who were tested in 1997 as 10-12 year-olds and again in 2002 as 15-17-year-olds. The set from the U.K. included 3,677 children who were tested in 1980 as 10-year-olds and in 1986 as 16-year-olds.

You can watch a short video of Siegler discussing the study and its implications at http://youtu.be/7YSj0mmjwBM.

Spatial skills improve children’s number sense

More support for the idea that honing spatial skills leads to better mathematical ability comes from a new children’s study.

The study found that first- and second-graders with the strongest spatial skills at the beginning of the school year showed the most improvement in their number line sense over the course of the year. Similarly, in a second experiment, not only were those children with better spatial skills at 5 ½ better on a number-line test at age 6, but this number line knowledge predicted performance on a math estimation task at age 8.

Hasty answers may make boys better at math

A study following 311 children from first to sixth grade has revealed gender differences in their approach to math problems. The study used single-digit addition problems, and focused on the strategy of directly retrieving the answer from long-term memory.

Accurate retrieval in first grade was associated with working memory capacity and intelligence, and predicted a preference for direct retrieval in second grade. However, at later grades the relation reversed, such that preference in one grade predicted accuracy and speed in the next grade.

Unlike girls, boys consistently preferred to use direct retrieval, favoring speed over accuracy. In the first and second grades, this was seen in boys giving more answers in total, and more wrong answers. Girls, on the other hand, were right more often, but responded less often and more slowly. By sixth grade, however, the boys’ practice was paying off, and they were both answering more problems and getting more correct.

In other words, while ability was a factor in early skilled retrieval, the feedback loop of practice and skill leads to practice eventually being more important than ability — and the relative degrees of practice may underlie some of the gender differences in math performance.

The findings also add weight to the view being increasingly expressed, that mistakes are valuable and educational approaches that try to avoid mistakes (e.g., errorless learning) should be dropped.

Infants can’t compare big and small groups

Our brains process large and small numbers of objects using two different mechanisms, seen in the ability to estimate numbers of items at a glance and the ability to visually track small sets of objects. A new study indicates that at age one, infants can’t yet integrate those two processes. Accordingly, while they can choose the larger of two sets of items when both sets are larger or smaller than four, they can’t distinguish between a large (above four) and small (below four) set.

In the study, infants consistently chose two food items over one and eight items over four, but chose randomly when asked to compare two versus four and two versus eight.

The researchers suggest that educational programs that claim to give children an advantage by teaching them arithmetic at an early age are unlikely to be effective for this reason.

Genetic analysis of 9,232 older adults (average age 67; range 56-84) has implicated four genes in how fast your hippocampus shrinks with age (rs7294919 at 12q24, rs17178006 at 12q14, rs6741949 at 2q24, rs7852872 at 9p33). The first of these (implicated in cell death) showed a particularly strong link to a reduced hippocampus volume — with average consequence being a hippocampus of the same size as that of a person 4-5 years older.

Faster atrophy in this crucial brain region would increase people’s risk of Alzheimer’s and cognitive decline, by reducing their cognitive reserve. Reduced hippocampal volume is also associated with schizophrenia, major depression, and some forms of epilepsy.

In addition to cell death, the genes linked to this faster atrophy are involved in oxidative stress, ubiquitination, diabetes, embryonic development and neuronal migration.

A younger cohort, of 7,794 normal and cognitively compromised people with an average age of 40, showed that these suspect gene variants were also linked to smaller hippocampus volume in this age group. A third cohort, comprised of 1,563 primarily older people, showed a significant association between the ASTN2 variant (linked to neuronal migration) and faster memory loss.

In another analysis, researchers looked at intracranial volume and brain volume in 8,175 elderly. While they found no genetic associations for brain volume (although there was one suggestive association), they did discover that intracranial volume (the space occupied by the fully developed brain within the skull — this remains unchanged with age, reflecting brain size at full maturity) was significantly associated with two gene variants (at loci rs4273712, on chromosome 6q22, and rs9915547, on 17q21). These associations were replicated in a different sample of 1,752 older adults. One of these genes is already known to play a unique evolutionary role in human development.

A meta-analysis of seven genome-wide association studies, involving 10,768 infants (average age 14.5 months), found two loci robustly associated with head circumference in infancy (rs7980687 on chromosome 12q24 and rs1042725 on chromosome 12q15). These loci have previously been associated with adult height, but these effects on infant head circumference were largely independent of height. A third variant (rs11655470 on chromosome 17q21 — note that this is the same chromosome implicated in the study of older adults) showed suggestive evidence of association with head circumference; this chromosome has also been implicated in Parkinson's disease and other neurodegenerative diseases.

Previous research has found an association between head size in infancy and later development of Alzheimer’s. It has been thought that this may have to do with cognitive reserve.

Interestingly, the analyses also revealed that a variant in a gene called HMGA2 (rs10784502 on 12q14.3) affected intelligence as well as brain size.

Why ‘Alzheimer’s gene’ increases Alzheimer’s risk

Investigation into the so-called ‘Alzheimer’s gene’ ApoE4 (those who carry two copies of this variant have roughly eight to 10 times the risk of getting Alzheimer’s disease) has found that ApoE4 causes an increase in cyclophilin A, which in turn causes a breakdown of the cells lining the blood vessels. Blood vessels become leaky, making it more likely that toxic substances will leak into the brain.

The study found that mice carrying the ApoE4 gene had five times as much cyclophilin A as normal, in cells crucial to maintaining the integrity of the blood-brain barrier. Blocking the action of cyclophilin A brought blood flow back to normal and reduced the leakage of toxic substances by 80%.

The finding is in keeping with the idea that vascular problems are at the heart of Alzheimer’s disease — although it should not be assumed from that, that other problems (such as amyloid-beta plaques and tau tangles) are not also important. However, one thing that does seem clear now is that there is not one single pathway to Alzheimer’s. This research suggests a possible treatment approach for those carrying this risky gene variant.

Note also that this gene variant is not only associated with Alzheimer’s risk, but also Down’s syndrome dementia, poor outcome following TBI, and age-related cognitive decline.

On which note, I’d like to point out recent findings from the long-running Nurses' Health Study, involving 16,514 older women (70-81), that suggest that effects of postmenopausal hormone therapy for cognition may depend on apolipoprotein E (APOE) status, with the fastest rate of decline being observed among HT users who carried the APOe4 variant (in general HT was associated with poorer cognitive performance).

It’s also interesting to note another recent finding: that intracranial volume modifies the effect of apoE4 and white matter lesions on dementia risk. The study, involving 104 demented and 135 nondemented 85-year-olds, found that smaller intracranial volume increased the risk of dementia, Alzheimer's disease, and vascular dementia in participants with white matter lesions. However, white matter lesions were not associated with increased dementia risk in those with the largest intracranial volume. But intracranial volume did not modify dementia risk in those with the apoE4 gene.

More genes involved in Alzheimer’s

More genome-wide association studies of Alzheimer's disease have now identified variants in BIN1, CLU, CR1 and PICALM genes that increase Alzheimer’s risk, although it is not yet known how these gene variants affect risk (the present study ruled out effects on the two biomarkers, amyloid-beta 42 and phosphorylated tau).

Same genes linked to early- and late-onset Alzheimer's

Traditionally, we’ve made a distinction between early-onset Alzheimer's disease, which is thought to be inherited, and the more common late-onset Alzheimer’s. New findings, however, suggest we should re-think that distinction. While the genetic case for early-onset might seem to be stronger, sporadic (non-familial) cases do occur, and familial cases occur with late-onset.

New DNA sequencing techniques applied to the APP (amyloid precursor protein) gene, and the PSEN1 and PSEN2 (presenilin) genes (the three genes linked to early-onset Alzheimer's) has found that rare variants in these genes are more common in families where four or more members were affected with late-onset Alzheimer’s, compared to normal individuals. Additionally, mutations in the MAPT (microtubule associated protein tau) gene and GRN (progranulin) gene (both linked to frontotemporal dementia) were also found in some Alzheimer's patients, suggesting they had been incorrectly diagnosed as having Alzheimer's disease when they instead had frontotemporal dementia.

Of the 439 patients in which at least four individuals per family had been diagnosed with Alzheimer's disease, rare variants in the 3 Alzheimer's-related genes were found in 60 (13.7%) of them. While not all of these variants are known to be pathogenic, the frequency of mutations in these genes is significantly higher than it is in the general population.

The researchers estimate that about 5% of those with late-onset Alzheimer's disease have changes in these genes. They suggest that, at least in some cases, the same causes may underlie both early- and late-onset disease. The difference being that those that develop it later have more protective factors.

Another gene identified in early-onset Alzheimer's

A study of the genes from 130 families suffering from early-onset Alzheimer's disease has found that 116 had mutations on genes already known to be involved (APP, PSEN1, PSEN2 — see below for some older reports on these genes), while five of the other 14 families all showed mutations on a new gene: SORL1.

I say ‘new gene’ because it hasn’t been implicated in early-onset Alzheimer’s before. However, it has been implicated in the more common late-onset Alzheimer’s, and last year a study reported that the gene was associated with differences in hippocampal volume in young, healthy adults.

The finding, then, provides more support for the idea that some cases of early-onset and late-onset Alzheimer’s have the same causes.

The SORL1 gene codes for a protein involved in the production of the beta-amyloid peptide, and the mutations seen in this study appear to cause an under-expression of SORL1, resulting in an increase in the production of the beta-amyloid peptide. Such mutations were not found in the 1500 ethnicity-matched controls.

 

Older news reports on these other early-onset genes (brought over from the old website):

New genetic cause of Alzheimer's disease

Amyloid protein originates when it is cut by enzymes from a larger precursor protein. In very rare cases, mutations appear in the amyloid precursor protein (APP), causing it to change shape and be cut differently. The amyloid protein that is formed now has different characteristics, causing it to begin to stick together and precipitate as amyloid plaques. A genetic study of Alzheimer's patients younger than 70 has found genetic variations in the promoter that increases the gene expression and thus the formation of the amyloid precursor protein. The higher the expression (up to 150% as in Down syndrome), the younger the patient (starting between 50 and 60 years of age). Thus, the amount of amyloid precursor protein is a genetic risk factor for Alzheimer's disease.

Theuns, J. et al. 2006. Promoter Mutations That Increase Amyloid Precursor-Protein Expression Are Associated with Alzheimer Disease. American Journal of Human Genetics, 78, 936-946.

http://www.eurekalert.org/pub_releases/2006-04/vfii-rda041906.php

Evidence that Alzheimer's protein switches on genes

Amyloid b-protein precursor (APP) is snipped apart by enzymes to produce three protein fragments. Two fragments remain outside the cell and one stays inside. When APP is produced in excessive quantities, one of the cleaved segments that remains outside the cell, called the amyloid b-peptides, clumps together to form amyloid plaques that kill brain cells and may lead to the development of Alzheimer’s disease. New research indicates that the short "tail" segment of APP that is trapped inside the cell might also contribute to Alzheimer’s disease, through a process called transcriptional activation - switching on genes within the cell. Researchers speculate that creation of amyloid plaque is a byproduct of a misregulation in normal APP processing.

[2866] Cao X, Südhof TC. A Transcriptively Active Complex of APP with Fe65 and Histone Acetyltransferase Tip60. Science [Internet]. 2001 ;293(5527):115 - 120. Available from: http://www.sciencemag.org/content/293/5527/115

http://www.eurekalert.org/pub_releases/2001-07/aaft-eta070201.php

Inactivation of Alzheimer's genes in mice causes dementia and brain degeneration

Mutations in two related genes known as presenilins are the major cause of early onset, inherited forms of Alzheimer's disease, but how these mutations cause the disease has not been clear. Since presenilins are involved in the production of amyloid peptides (the major components of amyloid plaques), it was thought that such mutations might cause Alzheimer’s by increasing brain levels of amyloid peptides. Accordingly, much effort has gone into identifying compounds that could block presenilin function. Now, however, genetic engineering in mice has revealed that deletion of these genes causes memory loss and gradual death of nerve cells in the mouse brain, demonstrating that the protein products of these genes are essential for normal learning, memory and nerve cell survival.

Saura, C.A., Choi, S-Y., Beglopoulos, V., Malkani, S., Zhang, D., Shankaranarayana Rao, B.S., Chattarji, S., Kelleher, R.J.III, Kandel, E.R., Duff, K., Kirkwood, A. & Shen, J. 2004. Loss of Presenilin Function Causes Impairments of Memory and Synaptic Plasticity Followed by Age-Dependent Neurodegeneration. Neuron, 42 (1), 23-36.

http://www.eurekalert.org/pub_releases/2004-04/cp-ioa032904.php

[2858] Consortium ENIGM-A (ENIGMA), Cohorts Heart Aging Research Genomic Epidemiology (charge). Common variants at 12q14 and 12q24 are associated with hippocampal volume. Nature Genetics [Internet]. 2012 ;44(5):545 - 551. Available from: http://www.nature.com/ng/journal/v44/n5/full/ng.2237.html

[2909] Taal RH, Pourcain BS, Thiering E, Das S, Mook-Kanamori DO, Warrington NM, Kaakinen M, Kreiner-Møller E, Bradfield JP, Freathy RM, et al. Common variants at 12q15 and 12q24 are associated with infant head circumference. Nature Genetics [Internet]. 2012 ;44(5):532 - 538. Available from: http://www.nature.com/ng/journal/v44/n5/abs/ng.2238.html

[2859] Cohorts Heart Aging Research Genomic Epidemiology (charge), Consortium EGG (EGG). Common variants at 6q22 and 17q21 are associated with intracranial volume. Nature Genetics [Internet]. 2012 ;44(5):539 - 544. Available from: http://www.nature.com/ng/journal/v44/n5/full/ng.2245.html

[2907] Stein JL, Medland SE, Vasquez AA, Hibar DP, Senstad RE, Winkler AM, Toro R, Appel K, Bartecek R, Bergmann Ø, et al. Identification of common variants associated with human hippocampal and intracranial volumes. Nature Genetics [Internet]. 2012 ;44(5):552 - 561. Available from: http://www.nature.com/ng/journal/v44/n5/abs/ng.2250.html

[2925] Bell RD, Winkler EA, Singh I, Sagare AP, Deane R, Wu Z, Holtzman DM, Betsholtz C, Armulik A, Sallstrom J, et al. Apolipoprotein E controls cerebrovascular integrity via cyclophilin A. Nature [Internet]. 2012 . Available from: http://www.nature.com/nature/journal/vaop/ncurrent/full/nature11087.html?WT.ec_id=NATURE-20120517

Kang, J. H., & Grodstein F. (2012).  Postmenopausal hormone therapy, timing of initiation, APOE and cognitive decline. Neurobiology of Aging. 33(7), 1129 - 1137.

Skoog, I., Olesen P. J., Blennow K., Palmertz B., Johnson S. C., & Bigler E. D. (2012).  Head size may modify the impact of white matter lesions on dementia. Neurobiology of Aging. 33(7), 1186 - 1193.

[2728] Cruchaga C, Chakraverty S, Mayo K, Vallania FLM, Mitra RD, Faber K, Williamson J, Bird T, Diaz-Arrastia R, Foroud TM, et al. Rare Variants in APP, PSEN1 and PSEN2 Increase Risk for AD in Late-Onset Alzheimer's Disease Families. PLoS ONE [Internet]. 2012 ;7(2):e31039 - e31039. Available from: UR - http://dx.doi.org/10.1371/journal.pone.0031039,http://dx.doi.org/10.1371/journal.pone.0031039

Full text available at http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0031039

[2897] Pottier C, Hannequin D, Coutant S, Rovelet-Lecrux A, Wallon D, Rousseau S, Legallic S, Paquet C, Bombois S, Pariente J, et al. High frequency of potentially pathogenic SORL1 mutations in autosomal dominant early-onset Alzheimer disease. Molecular Psychiatry [Internet]. 2012 . Available from: http://www.nature.com/mp/journal/vaop/ncurrent/full/mp201215a.html

McCarthy, J. J., Saith S., Linnertz C., Burke J. R., Hulette C. M., Welsh-Bohmer K. A., et al. (2012).  The Alzheimer's associated 5′ region of the SORL1 gene cis regulates SORL1 transcripts expression. Neurobiology of Aging. 33(7), 1485.e1-1485.e8 - 1485.e1-1485.e8

Iron deficiency is the world's single most common nutrient deficiency, and a well-known cause of impaired cognitive, language, and motor development. Many countries therefore routinely supplement infant foods with iron. However, a new study suggests that, while there is no doubt that such fortification has helped reduce iron deficiency, it may be that there is an optimal level of iron for infant development.

In 1992-94, 835 healthy, full-term infants living in urban areas in Chile, took part in a randomized trial to receive iron-fortified formula from 6 months of age to 12 months. A follow-up study has now assessed the cognitive functioning of 473 of these children at 10 years of age. Tests measured IQ, spatial memory, arithmetic achievement, visual-motor integration, visual perception and motor functioning.

Those who had received iron-fortified formula scored significantly lower than the non-fortified group on the spatial memory and visual-motor integration tests. Moreover, their performance on the other tests also tended to be worse, although these didn’t reach statistical significance.

There was no difference in iron level between these two groups (at age 10), and only one child had iron-deficiency anemia.

The crucial point, it seems, lies in the extent to which the infants needed additional iron. Children who had high iron levels at 6 months (5.5%, i.e. 26 infants) had lower scores at 10 years if they had received the iron-fortified formula, but those with low 6-month iron levels (18.4%; 87 infants) had higher scores at 10 years.

Further research is needed to confirm these findings, but the findings are not inconsistent with the idea that iron overload promotes neurodegenerative diseases.

In another longitudinal study, brain scans have revealed that teenage iron levels are associated with white matter fiber integrity.

The study first measured iron levels in 615 adolescent twins and siblings, and then scanned their brains when they were in their early twenties. Myelin (white matter) contains a lot of iron, so the strong correlation between teenage iron level and white matter integrity in young adulthood is not unexpected.

The correlation was stronger between identical twins that non-identical twins, suggesting a genetic contribution. Again, not unexpected — the transport of iron around the body is affected by several genes. One particular gene variant, in a gene that governs cellular absorption of transferrin-bound iron, was associated with both high iron levels and improved white matter integrity. This gene variant is found in about 12-15% of Caucasians.

The vital missing bit of information (because it wasn’t investigated) is whether this gene variant is associated with better cognitive performance. Further research will hopefully also investigate whether, while it might be better to have this variant earlier in life, it is detrimental in old age, given the suggestions that iron accumulation contributes to some neurodegenerative disorders (including Alzheimer’s).

Our common difficulty in recognizing faces that belong to races other than our own (or more specifically, those we have less experience of) is known as the Other Race Effect. Previous research has revealed that six-month-old babies show no signs of this bias, but by nine months, their ability to recognize faces is reduced to those races they see around them.

Now, an intriguing study has looked into whether infants can be trained in such a way that they can maintain the ability to process other-race faces. The study involved 32 six-month-old Caucasian infants, who were shown picture books that contained either Chinese (training group) or Caucasian (control group) faces. There were eight different books, each containing either six female faces or six male faces (with names). Parents were asked to present the pictures in the book to their child for 2–3 minutes every day for 1 week, then every other day for the next week, and then less frequently (approximately once every 6 days) following a fixed schedule of exposures during the 3-month period (equating to approximately 70 minutes of exposure overall).

When tested at nine months, there were significant differences between the two groups that indicated that the group who trained on the Chinese faces had maintained their ability to discriminate Chinese faces, while those who had trained on the Caucasian faces had lost it (specifically, they showed no preference for novel or familiar faces, treating them both the same).

It’s worth noting that the babies generalized from the training pictures, all of which showed the faces in the same “passport photo” type pose, to a different orientation (three-quarter pose) during test trials. This finding indicates that infants were actually learning the face, not simply an image.

A new automated vocal analysis technology can discriminate pre-verbal vocalizations of very young children with autism with 86% accuracy. The LENA™ (Language Environment Analysis) system also differentiated typically developing children and children with autism from children with language delay. The processor fits into the pocket of specially designed children's clothing and records everything the child vocalizes. LENA could not only enable better early diagnosis of autism spectrum disorders, but also allow parents to continue and supplement language enrichment therapy at home and assess their own effectiveness for themselves.

Like human faces, infants are predisposed to pay attention to words. Now a new study shows that they learn concepts from them from a very early age. In the study, in which 46 three-month-old infants were shown a series of pictures of fish that were paired either with words (e.g., "Look at the toma!") or beeps (carefully matched to the words for tone and duration), those who heard the words subsequently showed signs of having formed the category “fish”, while those who heard the tones did not. Categorization was assumed when infants shown a picture of a new fish and a dinosaur side-by-side, looked longer at one picture than the other.

A guinea pig study has found that newborn guinea pigs subjected to moderate vitamin C deficiency had 30% fewer hippocampal neurons and markedly worse spatial memory than guinea pigs given a normal diet. For several reasons the neonatal brain is thought to be particularly vulnerable to even a slight lowering of the vitamin C level. Vitamin C deficiency is very common in some parts of the world, and even in wealthy nations occurs in an estimated 5-10% of the adult population.

The nutrient choline is known to play a critical role in memory and brain function by positively affecting the brain's physical development through increased production of stem cells (the parents of brain cells). New research demonstrates that this occurs through the effect of choline on the expression of particular genes. The important finding is that diet during pregnancy turns on or turns off division of stem cells that form the memory areas of the brain. Developing babies get choline from their mothers during pregnancy and from breast milk after they are born. Other foods rich in choline include eggs, meat, peanuts and dietary supplements. Breast milk contains much more of this nutrient than many infant formulas. Choline is a vitamin-like substance that is sometimes treated like B vitamins and folic acid in dietary recommendations.
A choline food database is available at: www.nal.usda.gov/fnic/foodcomp.

Older news items (pre-2010) brought over from the old website

New screening tool helps identify children at risk

An exam, called the NICU (neonatal intensive care unit) Network Neurobehavioral Scale (NNNS), has been created to identify newborns who may have problems with school readiness and behavior at age four. This opens up the possibility of early intervention to prevent these problems. The screening exam has been tested on 1248 babies, mostly black and on public assistance. Five discrete behavioral profiles were reliably identified; the most extreme negative profile was found in 5.8% of the infants. Infants with poor performance were more likely to have behavior problems at age three, school readiness problems at age four, and low IQ at 4 ½ — 40% had clinically significant problems externalizing (impulsivity and acting out), internalizing (anxiety, depression, withdrawn personalities), and with school readiness (delays in motor, concepts and language skills), and 35% had low IQ.

Liu, J., Bann, C., Lester, B., Tronick, E., Das, A., Lagasse, L., et al. (2010). Neonatal Neurobehavior Predicts Medical and Behavioral Outcome. Pediatrics, 125(1), e90-98. doi: 10.1542/peds.2009-0204.

http://www.eurekalert.org/pub_releases/2009-12/bu-nst120709.php

New view of the way young children think

It seems that young children neither plan for the future nor live completely in the present — rather they call up the past as they need it. A study in which 3 ½ year-olds and 8-year-olds played a computer game that involved teaching children simple rules about two cartoon characters and their preferences for different objects has found that 8 year olds had no trouble remembering the preferences and clicking either a happy or sad face when the character had an object they liked or disliked, but 3 year olds found the task difficult. Measuring pupil dilation (a reflection of mental effort), it was found that the older children found the sequence easy because they could anticipate the answer before the object appeared, but preschoolers waited until they saw the object. The researchers suggest that rather than repeat something again and again that requires a young child to prepare for something in advance, you should try to highlight the problem that they are going to have.

Chatham, C.H., Frank, M.J. & Munakata, Y. 2009. Pupillometric and behavioral markers of a developmental shift in the temporal dynamics of cognitive control. Proceedings of the National Academy of Sciences, 106, 5529-5533.

http://www.eurekalert.org/pub_releases/2009-03/uoca-crp032409.php
http://www.physorg.com/news157123504.html

Infants have limited ability to draw on past to understand other people's behavior

We know that providing advance information about the goal of instruction helps people learn. Now it appears that this is true even for infants, but they need the additional prompt of the same location. The study involved infants first being shown, five times, an assistant reach for and pick up one of two plastic toys while saying "Wow!" The infants were then randomly selected to stay in the same room or go to a different one. It was found that those who stayed in the same room were more likely to show surprise when the assistant changed her mind about which toy she wanted.

Sommerville, J.A. & Crane, C.C. 2009. Ten-month-old infants use prior information to identify an actor's goal. Developmental Science, 12 (2), 314-325.

http://www.physorg.com/news151853797.html
http://www.eurekalert.org/pub_releases/2009-01/uow-ido012209.php

Even toddlers can ‘chunk' information for better remembering

We all know it’s easier to remember a long number (say a phone number) when it’s broken into chunks. Now a study has found that we don’t need to be taught this; it appears to come naturally to us. The study showed 14 months old children could track only three hidden objects at once, in the absence of any grouping cues, demonstrating the standard limit of working memory. However, with categorical or spatial cues, the children could remember more. For example, when four toys consisted of two groups of two familiar objects, cats and cars, or when six identical orange balls were grouped in three groups of two.

Feigenson, L. & Halberda, J. 2008. Conceptual knowledge increases infants' memory capacity. Proceedings of the National Academy of Sciences, 105 (29), 9926-9930.

http://www.eurekalert.org/pub_releases/2008-07/jhu-etg071008.php

Toddlers can learn complex actions from picture-book reading

A study of preschool children has found picture books not only encourage reading development, but also help toddlers learn about the real world. However, very young children (18 months) were much less likely to be able to imitate specific target actions on novel real-world objects when the pictures were colored-pencil drawings rather than life-like color photographs.

Simcock, G. & DeLoache, J. 2006. Get the picture? The Effects of Iconicity on Toddlers' Reenactment from Picture Books. Developmental Psychology, 42 (6)

http://www.eurekalert.org/pub_releases/2006-11/apa-tlc103006.php

Psychological reasoning begins earlier than had been thought

According to conventional wisdom, babies don't begin to develop sophisticated psychological reasoning about people until they are about 4 years old. A study of 15-month-olds proves otherwise. The study used a non-verbal approach, for obvious reasons, and the researchers suggest earlier studies that found 3 year olds unable to reason about what others believe used verbal tasks that were overly complex for the young children.

Onishi, K.H. & Baillargeon, R. 2005. Do 15-Month-Old Infants Understand False Beliefs? Science, 308, 255-258.

http://www.eurekalert.org/pub_releases/2005-04/uoia-prb041405.php

Early learning leaves lasting changes in brain

An owl study points to the importance of early childhood education, by demonstrating that early learning experiences forever change the brain's structure. While some parts of the brain remain relatively flexible throughout life, other parts lose the ability to make large-scale changes in connections early in life. Those brain regions that help sense and interpret the world are most affected by early childhood experiences.

Linkenhoker, B.A., von der Ohe, C.G. & Knudsen, E.I. 2005. Anatomical traces of juvenile learning in the auditory system of adult barn owls. Nature Neuroscience, 8, 93 – 98.

http://www.eurekalert.org/pub_releases/2004-12/sumc-ell121704.php

Infants Don't Encode Long-Term Memories Until Second Year

It appears that the area of the brain thought to play a key role in encoding long-term memory matures in spurts. A new study demonstrates that a major spurt happens after a person's first year and then takes a second year to fully mature. Babies exposed to a series of actions when they were 9, 17 or 24 months old, were tested four months later. Those babies who had been 17 or 24 months old recalled the actions well, but the younger babies didn’t. The dramatic growth that occurs in the brain between 8 and 12 months may be required for long-term memory.

Liston, C. &Kagan, J. 2002. Brain development: Memory enhancement in early childhood. Nature, 419 (6910), 896.