Researchers divided the infants into two equal groups: 22 were considered at high risk because at least one parent had ADHD, while 22 were at low risk because neither parent had the disorder. Parental ADHD status was established through semi-structured diagnostic interviews covering childhood and adult symptoms and impairment. This approach was more rigorous than relying only on self-reported symptoms or a single symptom threshold.

The infants came from the Pittsburgh ADHD Risk in Infancy Study, a longitudinal cohort designed to examine neurodevelopmental pathways associated with elevated ADHD risk. The team used functional near-infrared spectroscopy, or fNIRS, to measure brain activity noninvasively during a low-cognitive-load attention task. At 8–10 months and again at 12–14 months, infants watched a seven-minute abstract film designed to hold their attention with minimal demands.

Near-infrared light was directed toward the forehead and posterior parietal regions, allowing the researchers to infer changes in cortical activity from shifts in oxygenated and deoxygenated hemoglobin in cerebral blood. Functional connectivity was then estimated from the statistical relationships between signals recorded across those regions. This method has practical advantages for studying infancy.

Unlike functional magnetic resonance imaging, fNIRS can be performed while a child remains awake, is silent, and is less sensitive to movement artifacts. Those qualities allowed the investigators to repeat the assessment during a period when the brain is developing rapidly and attention is beginning to shift from stimulus-driven responses toward more voluntary control. The study examined the dorsal attention network and frontoparietal systems that support sustained attention and emerging executive control, including the dorsolateral prefrontal cortex, frontal eye fields, and parietal regions.

Across all 44 infants, connectivity strengthened in several frontal relationships as the participants moved from the first to the second assessment. Connections between the left dorsolateral prefrontal cortex and left frontal eye field increased, as did the link between left and right dorsolateral prefrontal regions. At the same time, connectivity between the right frontal eye field and right parietal cortex declined.

The researchers described this pattern as consistent with a leftward shift in frontal network organization, potentially reflecting the early specialization of systems involved in attention, although that interpretation remains a hypothesis about the observed trajectories. Familial risk was associated with localized rather than universal differences in connectivity. High-risk infants showed increases in several connections linking the left frontal eye field or left dorsolateral prefrontal cortex to the right parietal cortex.

By contrast, low-risk infants showed an increase in connectivity between the left and right dorsolateral prefrontal regions, alongside a decrease in the left prefrontal-to-right parietal connection and an increase in a right frontal eye field-to-left parietal connection. The clearest direct group difference was found in the left dorsolateral prefrontal cortex-to-right parietal cortex pathway: it increased over time in high-risk infants but decreased in low-risk infants, and this contrast survived false-discovery-rate correction. Two additional high-versus-low comparisons suggested larger changes involving the left frontal eye field, but those results did not survive correction for multiple comparisons.

The study therefore provides limited evidence that risk-related differences extend beyond the prefrontal-parietal pathway, and it should not be read as proof of a distinct ADHD brain network in infancy. The authors proposed that greater connectivity among high-risk infants might reflect early compensatory recruitment of additional neural resources to support attention. An alternative interpretation is that the same pattern reflects difficulty filtering relevant from irrelevant information.

The observational design cannot distinguish these possibilities or show that altered connectivity causes later symptoms. Parents also rated their children’s behavior when the infants were 18–29.9 months old, using the Child Behavior Checklist’s DSM-oriented ADHD Problems scale. High-risk toddlers had higher average scores than low-risk toddlers: 4.0 versus 1.7.

Only one child, in the high-risk group, scored in the borderline or clinical range, and neither group was characterized by high levels of reported ADHD-related behavior overall. Within the full sample, greater attention-related symptoms were associated at the uncorrected level with increases in several frontoparietal connections and with a decrease in communication between the left frontal eye field and right dorsolateral prefrontal cortex. None of these symptom associations remained significant after multiple-comparison correction.

The findings suggest that patterns associated with familial ADHD risk may be detectable before a formal ADHD diagnosis can be made, but the study is far from establishing an infant screening tool. Its final sample was modest, with 15 of 59 originally recruited infants excluded because of fussing or crying, technical error, or missing second-visit data. Functional brain networks are especially unstable during infancy, and the two visits covered age ranges rather than identical ages, adding variability to estimates of developmental change.

Risk was also defined by parental ADHD rather than an infant diagnosis, and many offspring at familial risk have typical development. Because the behavioral assessments occurred before the age at which ADHD can be diagnosed, the study cannot determine whether the imaging patterns predict a later diagnosis or merely reflect early familial and behavioral differences. Even so, the study’s longitudinal design and low-burden imaging method offer a way to observe how attention networks change during a sensitive developmental period.

Its main conclusion is carefully bounded: in this small cohort, familial ADHD risk was preliminarily associated with an altered trajectory of frontoparietal connectivity during the first year of life, while the link between infant connectivity and later ADHD-related behavior remains suggestive rather than conclusive.

Subject of Research: Longitudinal infant brain connectivity and familial risk for attention-deficit/hyperactivity disorder

Article Title: Familial risk for attention-deficit/hyperactivity disorder and related behaviors in toddlerhood are preliminarily associated with altered frontoparietal development in infancy measured by functional near-infrared spectroscopy

Article References: Krishnamurthy, M., Morgan, J. K., Santosa, H., Wilson, M. A., Huppert, T. J., & Joseph, H. M. (2026). Familial risk for attention-deficit/hyperactivity disorder and related behaviors in toddlerhood are preliminarily associated with altered frontoparietal development in infancy measured by functional near-infrared spectroscopy. Frontiers in Neuroscience, 20, Article 1919928. https://doi.org/10.3389/fnins.2026.1919928

Image Credits: AI Generated

DOI: 10.3389/fnins.2026.1919928

Keywords: ADHD, infant brain development, familial risk, frontoparietal network, functional near-infrared spectroscopy, neural connectivity, early childhood, longitudinal study, toddler behavior, Familial, risk, attention-deficit