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@ARTICLE{Leone:280972,
      author       = {Leone, Riccardo and Kobeleva, Xenia},
      collaboration = {Initiative, Alzheimer's Disease Neuroimaging},
      title        = {{W}hite matter hyperintensities contribute to early
                      cortical thinning in addition to tau in aging.},
      journal      = {Neurobiology of aging},
      volume       = {155},
      issn         = {0197-4580},
      address      = {Amsterdam [u.a.]},
      publisher    = {Elsevier Science},
      reportid     = {DZNE-2025-01054},
      pages        = {66 - 77},
      year         = {2025},
      abstract     = {White matter hyperintensities (WMH) are associated with
                      cortical thinning in distant brain regions. However, it is
                      currently unclear how WMH affect neurodegeneration in early
                      Alzheimer's disease (AD). Here, we investigated associations
                      between WMH and cortical thickness in temporal regions
                      involved in early AD (AD cortical signature), while
                      correcting for regional amyloid and tau accumulation
                      assessed by PET. We performed cross-sectional (n = 551), and
                      longitudinal (n = 125) analyses in older adults without
                      dementia, also stratified by amyloid positivity. We
                      evaluated WMH volume - as a measure of the global burden of
                      WMH-related cerebrovascular pathology (GB-WMH) - and
                      investigated the role of deep versus periventricular WMH. We
                      also tested whether a higher focal burden of WMH in specific
                      tracts connected to AD signature regions (FB-WMH) would lead
                      to greater cortical thinning than expected solely from
                      GB-WMH. We performed exploratory analyses in other brain
                      regions to check the specificity of our findings to the
                      temporal AD signature. GB-WMH damage, especially involving
                      periventricular WMH, was cross-sectionally (not
                      longitudinally) associated with cortical thinning in the
                      fusiform, inferior and middle temporal gyri. Stronger
                      associations were found in amyloid-positive individuals,
                      including for the entorhinal cortex. Effects were mostly
                      confined to regions of the temporal AD signature. FB-WMH did
                      not yield higher cortical thinning than expected solely by
                      GB-WMH. Cerebrovascular disease is associated with cortical
                      thinning of temporal regions involved in early AD.
                      Interventions aimed at improving cerebrovascular health
                      might help to mitigate neurodegeneration in these regions.},
      keywords     = {AD (Other) / Alzheimer’s Disease (Other) / Amyloid
                      (Other) / Copathologies (Other) / Cortical thickness (Other)
                      / Disconnections (Other) / Tau (Other) / WMH (Other)},
      cin          = {Clinical Research (Bonn) / AG Spottke},
      ddc          = {610},
      cid          = {I:(DE-2719)1011001 / I:(DE-2719)1011103},
      pnm          = {353 - Clinical and Health Care Research (POF4-353)},
      pid          = {G:(DE-HGF)POF4-353},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40712373},
      doi          = {10.1016/j.neurobiolaging.2025.07.007},
      url          = {https://pub.dzne.de/record/280972},
}