% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Schulze:285454,
      author       = {Schulze, Marcel and Autenrieth, Erik and Aslan, Behrem and
                      Stirnberg, Rüdiger and Stoecker, Tony and Lux, Silke and
                      Coghill, David and Silk, Tim and Philipsen, Alexandra},
      title        = {{Q}uantitative susceptibility mapping of brain iron in
                      adult {ADHD}.},
      journal      = {Frontiers in psychiatry},
      volume       = {17},
      issn         = {1664-0640},
      address      = {Lausanne},
      publisher    = {Frontiers Research Foundation},
      reportid     = {DZNE-2026-00236},
      pages        = {1735191},
      year         = {2026},
      abstract     = {Attention-deficit/hyperactivity disorder (ADHD) is a
                      neurodevelopmental condition that frequently persists into
                      adulthood and is linked to alterations in fronto-striatal
                      circuitry and dopaminergic signaling. Brain iron is
                      essential for dopamine synthesis and neural metabolism and
                      can be indexed in vivo using quantitative susceptibility
                      mapping (QSM), which reflects regional magnetic
                      susceptibility. Pediatric studies have mostly reported
                      reduced tissue iron susceptibility in ADHD, but data in
                      adults are limited. This study investigated regional
                      susceptibility in adults with ADHD, its relationship to
                      current and retrospective ADHD symptoms, and
                      depression.Twenty-five adults with ADHD and 24 healthy
                      controls underwent 3T MRI, including high-resolution QSM.
                      Mean susceptibility was extracted from 89 cortical and
                      subcortical regions of interest. For each ROI, group effects
                      were estimated using linear regression with
                      heteroskedasticity-consistent (HC3) inference. To account
                      for group differences in depressive symptoms, additional
                      models included Beck Depression Inventory (BDI-II) scores.
                      Dimensional associations with ADHD symptoms were tested
                      using covariate-adjusted ROI-symptom correlations for
                      current symptoms (CAARS) and retrospective childhood
                      symptoms (WURS-k). Benjamini-Hochberg false discovery rate
                      (FDR) correction was applied within each analysis across
                      ROIs.No ADHD-control group difference survived FDR
                      correction in any model. At the uncorrected level, adults
                      with ADHD showed lower susceptibility in ventral temporal
                      and posterior midline regions, most consistently in the
                      fusiform gyrus and posterior cingulate cortex
                      (small-to-moderate effect sizes across models). When
                      additionally adjusting for depressive symptoms, nominal
                      group differences remained confined to ventral
                      temporal/temporo-limbic and orbitofrontal regions (fusiform,
                      entorhinal cortex, medial orbitofrontal cortex), but again
                      did not survive FDR. Covariate-adjusted ROI-symptom
                      associations did not meet FDR significance; nominally,
                      higher ADHD symptom burden (particularly impulsivity) was
                      associated with lower susceptibility in posterior midline
                      regions (posterior cingulate, precuneus) and ventral
                      temporal cortex (fusiform).In this adult sample, QSM
                      provided no robust evidence for widespread or regionally
                      specific alterations in brain iron susceptibility in ADHD
                      after multiple-comparison correction. Nevertheless, the
                      reproducible pattern of nominal effects-centered on ventral
                      temporal and default-mode network hub regions-suggests that
                      inter-individual variation in cortical susceptibility may
                      relate to clinical heterogeneity and neurodevelopmental
                      timing rather than constituting a strong diagnostic
                      signature. Larger, medication-stratified and developmentally
                      informed studies are needed to clarify whether subtle
                      iron-related susceptibility patterns track symptom
                      dimensions, treatment exposure, and longitudinal
                      trajectories.},
      keywords     = {ADHD (Other) / QSM (Other) / brain iron (Other) /
                      neurodevelopment (Other) / symptom-coupling (Other)},
      cin          = {AG Stöcker},
      ddc          = {610},
      cid          = {I:(DE-2719)1013026},
      pnm          = {354 - Disease Prevention and Healthy Aging (POF4-354)},
      pid          = {G:(DE-HGF)POF4-354},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41767150},
      pmc          = {pmc:PMC12946022},
      doi          = {10.3389/fpsyt.2026.1735191},
      url          = {https://pub.dzne.de/record/285454},
}