Adult Influences on Early Language Development, Brain Myelination
Laia Fibla, Samuel H. Forbes, Jordan McCarthy, Kate Mee, Vincent Magnotta, et al.
(see pages 4279–4290)
Babies who hear more language input from adults at home at early ages develop more complex language abilities as children and, later on, higher literary skills. One thesis in the field is that socioeconomic status (SES) might be a major driver of increased language learning, but even within individual SES strata, kids develop differently. This week, Fibla et al. dive into the relationship among language exposure, SES, and structural brain development during development. Participants were children aged 6 months, a time of highly plastic brain activity before language development, and 30 months, when most children have a sizable vocabulary and myelination is well under way. SES is a complex multifactorial measure of a family's social and financial resources, often reflected by parental education and income. In this case, the authors derived SES from the mother's education level. The researchers used a language recording and analysis system called Language Environment Analysis (LENA) to measure children's language exposure at home. Children with higher SES heard more adult words and increased their vocalizations with age. The authors also used a specialized form of magnetic resonance imaging to examine myelin concentration in two language-associated brain areas: the arcuate fasciculus (AF) and the superior longitudinal fasciculus (SLF). Children in the older group (30 months of age) who had more exposure to adult speech showed higher concentrations of myelin in the AF and SLF. Unexpectedly, the opposite pattern was observed in younger children, with a negative association between myelination and adult input, but the authors caution that the finding is difficult to interpret because myelin levels are so low at 6 months. In a wider look at 17 language-associated brain regions, the researchers saw a similar pattern of increased myelin with higher adult input in older children, but a negative association in 6-month-old children. The study deepens our understanding of the codevelopment of language skill and brain myelination during early development.
A toddler wears a LENA device like that used by Fibla et al. to record and analyze adult and child language vocalizations.
VGLUT3 Transporter Modifies Huntington's Disease Progression
Karim S. Ibrahim, Salah El Mestikawy, Khaled S. Abd-Elrahman, and Stephen S. G. Ferguson
(see pages 4365–4377)
Huntington's disease (HD) is a fatal neurodegenerative disease caused by expansion of a polyglutamine repeat in the HTT gene, which encodes huntingtin, a large ubiquitous protein with uncertain function. The zQ175 mouse model of HD mimics the mutation seen in humans and displays the disease's hallmark progressive motor and cognitive symptoms. Although huntingtin is expressed throughout the brain and body, the pathophysiology of HD is most striking in the basal ganglia, including the striatum. In this week's issue, Ibrahim et al. focus on the vesicular glutamate transporter-3 (VGluT3), which regulates the striatal network and has been associated with other neuropsychiatric conditions but has not been investigated in the context of HD. The researchers crossed zQ175 mice with a VGluT3 knock-out mouse (zQ175:VGLUT3–/–). The loss of VGluT3 rescued the ability of mice to recognize novel objects at 12 and 15 months, and it improved the performance of mice on tests of motor coordination and grip strength, all of which were compromised in zQ175 mice. VGluT3 deletion did not, however, reverse the anxiogenic behavior seen in zQ175 mice; instead, it caused anxiety-like behavior in wild-type mice. In terms of pathophysiology, zQ175:VGLUT3–/– mice did not show the loss of NeuN-labeled neurons in the striatum seen in zQ175 mice at 15 months of age. Further, loss of VGLUT3 led to increased extracellular signal-related protein kinases that are disrupted by mutant HTT (mHTT) and in zQ175 mice, indicating a normalization. Disrupted autophagy was not rescued in the zQ175:VGLUT3–/– mice. In line with human pathophysiology, the zQ175 mice developed accumulation of mHTT and microgliosis in the dorsal striatum at 15 months. Interestingly, zQ175:VGLUT3–/– mice had a similar total number of mHTT aggregates, but nuclear aggregates were reduced compared with zQ175 mice. Microgliosis was not reduced by the loss of VGluT3. Together, the findings that VGluT3 deletion prevented short-term memory and motor declines and striatal neuron loss in a mouse model of HD points to the transporter as a key molecule in disease progression. The authors suggest that it may be a promising target for a disease-modifying treatment for HD.
Footnotes
This Week in The Journal was written by Stephani Sutherland
