In this study we explored the local and global changes in white matter of the brain and how these changes are associated in children between 9 and 12 years of age. We find that white matter volume increases (on average 6.0%), white matter surface area expands (on average 1.7%), and thickening and lengthening of fiber bundles occurs, during this three-year period. All fiber bundles showed an increase in their fractional anisotropy with increasing age (1.3% to 6.9%). Genes influence white matter volume (>80%), white matter surface (>80%) and fractional anisotropy in fiber bundles (up to 54%). The developmental changes in white matter volume and microstructure were explained by some (unknown) unique environmental factor.
We found white matter surface area expansion in the frontal, parietal and temporal lobes, between 9 and 12 years of age. Our findings at two specific ages helps to localize, in both space and time, the increase in white matter volume 
, mean surface area 
and expansion of fiber bundles 
that have been shown to occur in childhood and adolescence. Simultanously, fractional anisotropy increased in all the 14 major fiber bundles that we studied. Different rates of maturation have been suggested for different fiber bundles (e.g. 
) Our narrow age range makes it possible to pinpoint the changes that occur in a very specific time window. However, it does not allow for testing developmental trajectories over longer age-periods. The increases in fractional anisotropy found in our study are overall more widespread than those that have been found in voxel-based longitudinal studies in late adolescence and young adulthood 
. As these studies were done in somewhat older samples (age ranges 
, respectively), it is possible that white matter microstructure is developing at a rather global level in children at the brink of puberty and that only later, during puberty, differentiation in the developmental pattern occurs. However, the recent longitudinal tract-based study in subjects aged 5–32 years, showed an age-related increase in 10 of the major fiber bundles 
which is in line with our findings. Thus, we conclude that widespread age-related increases in fractional anisotropy occur between 9 and 12–years of age, although the extent is more prominent in some fiber bundles than in others.
The left arcuate fasciculus was the most prominently expanding fiber bundle of the 14 cortico-cortical fiber bundles between 9 and 12 years of age. Since the arcuate fasciculus is a bundle that is involved in language processing and young children have great potential to acquire new languages, we may speculate that the strengthening of the arcuate fasciculus is related to a stabilization of language skills. Indeed, the ability to acquire new languages diminishes fast after the age of 10 
. In addition, in the present study, prominent expansion was found in the splenium of the corpus callosum. The splenium contains the tracts involved in visual-spatial processing, which may be expected to develop early in life. Nevertheless, other studies too show prominent expansion in late childhood and young adolescence 
and increases in fractional anisotropy until early adolescence 
. It may be that the expansion occurring in our sample is related to bimanual coordination: during adolescence, both bimanual task performance and fractional anisotropy in the splenium increases 
Most likely, the continued expansion of white matter in childhood represents an increase in connectivity and reorganization throughout the brain. Based on post-mortem studies 
the increase in white matter volume is usually attributed to an increase in myelin (but see 
), thus representing an improvement in the speed of connections between anatomically distant brain areas. Our results indicate that white matter growth and fractional anisotropy increase cannot both be solely linked to myelination. While fractional anisotropy correlates with the thickness of myelin sheet 
, other factors such as compactness and organization of fiber bundles, and axonal diameter and density play a more prominent role (e.g. 
). In the mouse-model of the shiverer mouse that lacks myelin, fractional anisotropy is less affected by dysmyelination than other diffusion parameters, such as the trace 
. Although we can only speculate as to the underlying physiological processes underlying the development of white matter volume and microstructure, we hypothesize that the thickening of fiber bundles is not only the result from an increase of myelination, but also from an increase of axonal diameter and/or changes in the extracellular space. The latter two may negatively influence fractional anisotropy and their effects may temper the possible increase in fractional anisotropy due to increased myelination. Indeed, in pubertal rats, fractional anisotropy is positively correlated with the area of myelin sheath, but negatively with the extracellular space 
. Thus, the negative correlation between white matter growth and fractional anisotropy increase indicates that (at least) two different biological processes occur during white matter development. Myelination is likely one of them, but other processes influencing coherence of axonal bundles must also play a role. Future studies are warranted to investigate the relation between changes in white matter volume/surface area and fractional anisotropy at a local level.
White matter volume in 8 and 9 year old children is highly heritable 
. We show here for the first time that white matter surface area is also strongly influenced by genes. There are only two studies investigating genetic influences in white matter microstructure during puberty and adolescence: our previous study in the same cohort of 9-year olds showed moderate genetic influences in several of the major fiber bundles 
. A recent cross-sectional study comparing adolescents (12 and 16 year olds) to adults showed larger influences of genetic factors on fractional anisotropy in the younger group, indicating that heritability of white matter microstructure decreases with age, or environment increases its influence during life 
. In our longitudinal study we did not find this decrease in heritability, possibly due to our younger age, and much shorter time interval. The developmental changes in white matter volume and microstructure were explained by some (unknown) unique environmental factor. Whereas unique environmental factors always include measurement error, the existence of an environmental correlation (and the fact that both measurements were obtained from a different scan) shows that there must be some external factor influencing both white matter growth and increase in anisotropy of fiber bundles. Considering the growing importance of the unique environment on children once they reach puberty, the white matter changes may reflect adaptation of the brain at this age.