% 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{Benkarim:904400,
      author       = {Benkarim, Oualid and Paquola, Casey and Park, Bo-yong and
                      Hong, Seok-Jun and Royer, Jessica and Vos de Wael, Reinder
                      and Lariviere, Sara and Valk, Sofie and Bzdok, Danilo and
                      Mottron, Laurent and C. Bernhardt, Boris},
      title        = {{C}onnectivity alterations in autism reflect functional
                      idiosyncrasy},
      journal      = {Communications biology},
      volume       = {4},
      number       = {1},
      issn         = {2399-3642},
      address      = {London},
      publisher    = {Springer Nature},
      reportid     = {FZJ-2021-05970},
      pages        = {1078},
      year         = {2021},
      abstract     = {Autism spectrum disorder (ASD) is commonly understood as an
                      alteration of brain networks, yet case-control analyses
                      against typically-developing controls (TD) have yielded
                      inconsistent results. Here, we devised a novel approach to
                      profile the inter-individual variability in functional
                      network organization and tested whether such idiosyncrasy
                      contributes to connectivity alterations in ASD. Studying a
                      multi-centric dataset with 157 ASD and 172 TD, we obtained
                      robust evidence for increased idiosyncrasy in ASD relative
                      to TD in default mode, somatomotor and attention networks,
                      but also reduced idiosyncrasy in lateral temporal cortices.
                      Idiosyncrasy increased with age and significantly correlated
                      with symptom severity in ASD. Furthermore, while patterns of
                      functional idiosyncrasy were not correlated with ASD-related
                      cortical thickness alterations, they co-localized with the
                      expression patterns of ASD risk genes. Notably, we could
                      demonstrate that patterns of atypical idiosyncrasy in ASD
                      closely overlapped with connectivity alterations that are
                      measurable with conventional case-control designs and may,
                      thus, be a principal driver of inconsistency in the autism
                      connectomics literature. These findings support important
                      interactions between inter-individual heterogeneity in
                      autism and functional signatures. Our findings provide novel
                      biomarkers to study atypical brain development and may
                      consolidate prior research findings on the variable nature
                      of connectome level anomalies in autism.},
      cin          = {INM-7},
      ddc          = {570},
      cid          = {I:(DE-Juel1)INM-7-20090406},
      pnm          = {5252 - Brain Dysfunction and Plasticity (POF4-525)},
      pid          = {G:(DE-HGF)POF4-5252},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:34526654},
      UT           = {WOS:000696239600004},
      doi          = {10.1038/s42003-021-02572-6},
      url          = {https://juser.fz-juelich.de/record/904400},
}