ArticleMolecular psychiatry2021
Autophagy, apoptosis, and neurodevelopmental genes might underlie selective brain region vulnerability in attention-deficit/hyperactivity disorder.
Article in Molecular psychiatry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- Microbial biopriming of germinated barley enhances phenolics and B-vitamins and improves neurobehavior in MSG-treated rats.NPJ science of food · 2026Article
- TLR7 modulates glioblastoma progression through PI3K/AKT/mTOR pathway and immune microenvironment remodeling.Irish journal of medical science · 2026Article
- 3-Methyladenine administration alleviates cognitive and memory dysfunction in attention-deficit/hyperactivity disorder by modulating autophagy.Psychopharmacology · 2026Article
- Neurodevelopmental outcomes relevant to autism in juvenile mice exposed to PCB 11 in the maternal diet throughout gestation and lactation.Frontiers in toxicology · 2026Article
- Review
- Unraveling ADHD: genes, co-occurring traits, and developmental dynamics.Life science alliance · 2025Article
- Modulating Multiple Molecular Trajectories by Nutraceuticals and/or Physical Activity in Attention-Deficit/Hyperactivity Disorder (ADHD)-Like Behaviors in Rat Pups.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Article
- The relationship between sphingomyelin and ceramide levels and soft neurological signs in ADHD.Journal of neural transmission (Vienna, Austria : 1996) · 2025Article
- Pyriproxyfen, villain or good guy? A brief review.Archives of endocrinology and metabolism · 2024Review
- Polymorphism of Estrogen Receptor Genes and Its Interactions With Neurodevelopmental Genes in Attention Deficit Hyperactivity Disorder Among Chinese Han Descent.Psychiatry investigation · 2023Article
- Telencephalon Organoids Derived from an Individual with ADHD Show Altered Neurodevelopment of Early Cortical Layer Structure.Stem cell reviews and reports · 2023Article
- Construction of a Diagnostic Model and a lncRNA-Associated ceRNA Network Based on Apoptosis-Related Genes for Schizophrenia.Behavioural neurology · 2023Article
- Imaging Transcriptomics of Brain Disorders.Biological psychiatry global open science · 2022Review
- The placenta epigenome-brain axis: placental epigenomic and transcriptomic responses that preprogram cognitive impairment.Epigenomics · 2022Article
- Neuroplasticity to autophagy cross-talk in a therapeutic effect of physical exercises and irisin in ADHD.Frontiers in molecular neuroscience · 2022Review
- Consortium neuroscience of attention deficit/hyperactivity disorder and autism spectrum disorder: The ENIGMA adventure.Human brain mapping · 2022Review
- Prenatal Exposure to Triclocarban Impairs ESR1 Signaling and Disrupts Epigenetic Status in Sex-Specific Ways as Well as Dysregulates the Expression of Neurogenesis- and Neurotransmitter-Related Genes in the Postnatal Mouse Brain.International journal of molecular sciences · 2021Article
- The role of glucocorticoid receptor gene in the association between attention deficit-hyperactivity disorder and smaller brain structures.Journal of neural transmission (Vienna, Austria : 1996) · 2021Article
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5 authors.
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Abstract
Large-scale brain imaging studies by the ENIGMA Consortium identified structural changes associated with attention-deficit/hyperactivity disorder (ADHD). It is not clear why some brain regions are impaired and others spared by the etiological risks for ADHD. We hypothesized that spatial variation in brain cell organization and/or pathway expression levels contribute to selective brain region vulnerability (SBRV) in ADHD. In this study, we used the largest available collection of magnetic resonance imaging (MRI) results from the ADHD ENIGMA Consortium (subcortical MRI n = 3242; cortical MRI n = 4180) along with high-resolution postmortem brain microarray data from Allen Brain Atlas (donors n = 6) from 22 brain regions to investigate our SBRV hypothesis. We performed deconvolution of the bulk transcriptomic data to determine abundances of neuronal and nonneuronal cells in the brain. We assessed the relationships between gene-set expression levels, cell abundance, and standardized effect sizes representing regional changes in brain sizes in cases of ADHD. Our analysis yielded significant correlations between apoptosis, autophagy, and neurodevelopment genes with smaller brain sizes in ADHD, along with associations to regional abundances of astrocytes and oligodendrocytes. The lack of enrichment of common genetic risk variants for ADHD within implicated gene sets suggests an environmental etiology to these differences. This work provides novel mechanistic clues about SBRV in ADHD.
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