ArticlePsychological medicine2026
Cortical morphometric inverse divergence in attention-deficit/hyperactivity disorder correlates with cell-type-specific, laminar-specific and developmental transcriptomic signatures.
Article in Psychological medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
backgroundAttention-deficit/hyperactivity disorder (ADHD) is a neurodevelopmental condition with widespread brain structure alterations. However, the relationship between macroscale cortical organization and microscale molecular mechanisms remains unclear, particularly regarding the neurobiological mechanisms shared between the full ADHD cohort and its combined subtype (ADHD-C).
methodsWe analyzed 176 patients with ADHD (105 ADHD-C, 71 ADHD inattentive subtype) and 176 matched typically developing (TD) controls from the ADHD-200 dataset. Morphometric Inverse Divergence (MIND) networks quantified cortical similarity. Partial least squares (PLS) regression linked case-control MIND differences to cortical gene expression, assessing functional enrichment, cell-type specificity, and developmental trajectories.
resultsNeuroanatomically, the ADHD-C subtype exhibited widespread increases in regional MIND values, particularly in temporal and parietal cortices, reflecting greater inter-regional morphological homogeneity. PLS regression revealed that these MIND alterations were spatially correlated with a specific transcriptomic signature (PLS1+). These PLS1+ genes were significantly enriched in mitochondria-related metabolic pathways and showed distinct cortical layer specificity (notably layer V) and developmental stage specificity (from late fetal to late infancy stages). Regarding cell-type specificity, while PLS1+ genes in the full ADHD cohort were significantly enriched in excitatory and inhibitory neurons, the ADHD-C subtype showed similar but trend-level associations. Importantly, the full ADHD cohort and the ADHD-C group shared numerous PLS1-related genes and broad functional pathway enrichment commonalities.
conclusionsThis study links macroscale cortical abnormalities to microscale transcriptional regulation, with pronounced alterations in ADHD-C. The shared genetic and functional profiles between ADHD and its combined subtype underscore common pathological processes, providing novel insights into the neurodevelopmental mechanisms of ADHD.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.