Pubmed (TDAH) du 15/03/26
1. Pan S, Sun X, Xu S, Zhu H, Sun Y, Yu Y, Zhu J. Brain structures mediate the causal effects of socioeconomic status on mental disorders: A multi-stage Mendelian randomization study. J Affect Disord. 2026; 397: 120956.
BACKGROUND: The associations between socioeconomic status (SES), brain structural alterations, and mental disorders have been well established, but the causal nature and underlying mechanisms of such associations are elusive. METHODS: By performing multi-stage Mendelian randomization analyses of multi-source summary data from genome-wide association studies, we explored the causal associations of 3 SES indicators with 12 mental disorders and 13 types of brain structures, pursued by characterization of the mediating roles of brain structures in accounting for the causal effects of SES on mental disorders. RESULTS: Lower education attainment (EA), lower average total household income before tax (HIBT) and higher Townsend deprivation index at recruitment (TDI) were causally associated with an increased risk of many mental disorders such as attention deficit hyperactivity disorder, major depressive disorder, schizophrenia and cross-disorder, while higher EA, higher HIBT and lower TDI were causally associated with an increased risk of anorexia nervosa. Concurrently, lower EA and HIBT were causally linked to decreased surface area, cortical volume, folding index, intrinsic curvature and local gyrification index across a widely distributed set of cortical regions. More importantly, these brain structural alterations mediated the causal effects of lower EA and HIBT on the increased risk of attention deficit hyperactivity disorder, schizophrenia and cross-disorder. CONCLUSIONS: Our findings shed light on the neurobiological mechanisms whereby disadvantageous SES contributes to specific mental disorders, which may inform future preventive strategies for promoting resilience in high-risk individuals who are exposed to socioeconomic disadvantage.
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2. Tian T, Wang Y, Xu X, Li J, Feng J, Hu Y, Qi J. Preliminary exploration of the role and mechanism of BAIAP2 in learning and memory impairment in ADHD. Physiol Behav. 2026; 306: 115202.
Attention deficit hyperactivity disorder (ADHD), a highly prevalent neurodevelopmental disorder affecting children, presents with core symptoms of inattention, hyperactivity, and impulsivity, along with frequent comorbid learning and memory dysfunction. Emerging evidence implicates hippocampal dysfunction in ADHD-related learning and memory deficits, with brain-specific angiogenesis inhibitor 1-associated protein 2 (BAIAP2) emerging as a critical molecular player. While BAIAP2 has been independently associated with synaptic plasticity and ADHD pathogenesis, its specific role in ADHD-associated learning and memory impairment remains unexplored. Using spontaneously hypertensive rats (SHR), we demonstrated significantly reduced hippocampal BAIAP2 expression compared to controls. Notably, methylphenidate (MPH) treatment increased BAIAP2 levels, while targeted BAIAP2 overexpression rescued learning and memory deficits, as evidenced by Morris water maze (MWM) performance. Furthermore, we preliminarily explored the possible regulatory interactions between BAIAP2 and the long non-coding RNA lncNONRATT002035.2. These findings establish BAIAP2 as a pivotal mediator of hippocampal-dependent learning and memory dysfunction in ADHD and uncovered new aspects of disease pathology and potential targets for therapy.The newly discovered lncNONRATT002035.2-BAIAP2 axis warrants further investigation to elucidate its pathophysiological significance.
