Pubmed (TDAH) du 02/02/26
1. Chen MH, Chen LC, Hsu JW, Bai YM, Tsai SJ. Klotho as a novel biomarker of attention-deficit hyperactivity disorder and related executive dysfunction. BJPsych Open;2026 (Feb 2);12(2):e53.
BACKGROUND: Studies have shown that klotho, a neuroprotective protein, plays a crucial role in neurodevelopment. However, its association with attention-deficit hyperactivity disorder (ADHD), the most prevalent neurodevelopmental disorder, remains uncertain. AIMS: To elucidate klotho levels in adolescents with ADHD and to clarify its association with executive function. METHOD: The present study enrolled 92 adolescents (mean approximate age 14 years) diagnosed with ADHD and 80 age-matched healthy adolescents. All participants had their klotho levels measured and underwent the Wisconsin Card Sorting Test (WCST); their parents fulfilled the Swanson, Nolan and Pelham IV (SNAP-IV) scale and the Child Behavior Checklist-Dysregulation Profile (CBCL-DP). RESULTS: Results from generalised linear models (GLMs), with adjustments for age, gender, body mass index, clinical symptoms (SNAP-IV and CBCL-DP scores) and ADHD medication use, indicated that adolescents with ADHD had significantly lower klotho levels (P = 0.044) and performed worse on WCST (P = 0.027) compared with healthy adolescents. The GLMs further indicated a negative association between klotho levels and the percentage of non-perseverative errors on WCST (P = 0.002). CONCLUSIONS: Klotho may serve as a novel biomarker of ADHD and play a key role in ADHD-related executive dysfunction.
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2. Gonda X, Dome P, Balogh L, Baradits M, Réthelyi JM. Connecting the dots and finding the way forward: Pharmacological, neuromodulatory, and psychotherapeutic interventions for the complex treatment of adult ADHD. Pharmacol Ther;2026 (Jan 30):108997.
Attention-deficit/hyperactivity disorder (ADHD) persists into adulthood in up to 60% of cases, affecting 2.5-6.8% of adults worldwide, with high comorbidity rates of mood, anxiety, and substance use disorders, and significant functional impairments, such as reduced quality of life, increased mortality, and economic burden. This review synthesizes etiological factors, including neuroimaging evidence of fronto-striatal and default mode network disruptions, high heritability up to 70-80% driven by common, polygenic and rare variants, and environmental risk factors. Treatment emphasizes multimodal approaches, with stimulants as first-line pharmacotherapy due to their superior efficacy over non-stimulants like atomoxetine and viloxazine. Novel agents in development, such as centanafadine triple reuptake inhibitor and solriamfetol target core symptoms and comorbidities, showing promising phase III results. Despite the high effect sizes of pharmacological treatment for ADHD, obstacles such as acceptance and adherence remain challenging. Neuromodulatory interventions, including transcranial direct current stimulation (tDCS) and neurofeedback, demonstrate moderate effects on inattention and executive function. Psychotherapeutic options, particularly cognitive-behavioral therapy (CBT)-based interventions, improve symptom management and emotional regulation, often as adjuncts to medication. The review highlights the need for personalized strategies addressing adherence, comorbidity, and long-term outcomes, emphasizing integrated care to mitigate ADHD’s lifelong impact.
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3. Huang C, Kang Y, Peng R, Zhong H, Zeng N, Zhang L, Chen X, Du S. A novel de Novo KCNC1 mutation (c.1147 C > T) presenting with epilepsy and ADHD: a case report and literature review. BMC Neurol;2026 (Feb 2)
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4. Zhao Y, Zhang Y, Li T. Causal relationships between ADHD, ASD and brain structure: A mendelian randomization study. Prog Neuropsychopharmacol Biol Psychiatry;2026 (Jan 30):111631.
Neurodevelopmental disorders (NDDs) are debilitating conditions that impose significant burdens on individuals, families, and society. Despite evidence demonstrated altered brain structure in NDDs, definitive conclusions remain elusive. Using two-sample mendelian randomization (MR) and the latest GWAS findings, the current study aimed to elucidate the causal relationships between grey matter (GM), white matter (WM), subcortical regions, and two prevalent NDDs: attention deficit hyperactivity disorder (ADHD) and autism spectrum disorder (ASD). Our findings identified two frontal regions as key neural substrates in NDDs. Specifically, an increased surface area (SA) of the superior frontal gyrus (SFG) was significantly associated with an enhanced risk of ADHD (P = 2.04E-13, β = 4.28E-02, SE = 5.82E-03), while a larger SA of the orbital frontal gyrus (OFG) was associated with a reduced risk of ASD (P = 1.98E-42, β = -9.8E-02; SE = 0.007). Regarding WM tracts, the mode of anisotropy (MO) in the inferior fronto-occipital fasciculus (IFO) emerged as a causal factor for ADHD (P = 3.36E-70, β = -18.35; SE = 1.04), whereas the MO in the retro-lenticular part of the internal capsule (RLIC) was implicated in ASD (P = 1.37E-04, β = -12.73, SE = 3.34). No reverse causal link, i.e., brain alteration caused by NDDs was identified. Further mediation analyses using functional MRI (fMRI) GWAS data revealed that brain functional activities mediated the relationship between structural brain changes and NDDs risk. In conclusion, our findings underscored the critical role of the frontal lobe and association and projection fibers in the pathophysiology of NDDs, provide novel insights into the neural mechanisms underlying ADHD and ASD.
