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@ARTICLE{Ahmadi:1052289,
      author       = {Ahmadi, Reihaneh},
      title        = {{T}he {A}ssociation between {S}leep {D}isturbances,
                      {I}maging {B}iomarkers and {C}ognitive {D}ecline along the
                      {T}rajectory of {A}lzheimer's {D}isease},
      journal      = {Alzheimer's and dementia},
      volume       = {21},
      number       = {S2},
      issn         = {1552-5260},
      address      = {Hoboken, NJ},
      publisher    = {Wiley},
      reportid     = {FZJ-2026-00906},
      pages        = {e099181},
      year         = {2025},
      abstract     = {BackgroundAlzheimer's Disease (AD) is a prevalent and
                      debilitating neurodegenerative condition that significantly
                      impacts global health. Increasing evidence indicates that
                      sleep disturbances, including insomnia and Sleep-Disordered
                      Breathing (SDB), may act as modifiable risk factors for AD.
                      Despite extensive research into AD biomarkers, the complex
                      interactions between sleep disturbances, neuroimaging
                      biomarkers, and cognitive decline across the AD continuum
                      remain insufficiently explored. This study aimed to
                      investigate the relationships between self-reported sleep
                      disturbances, specifically insomnia and SDB, and imaging
                      biomarkers associated with AD.MethodData from 1510
                      participants in the Alzheimer's Disease Neuroimaging
                      Initiative (ADNI) were analyzed. Imaging biomarkers,
                      including tau and amyloid Positron Emission Tomography (PET)
                      and structural Magnetic Resonance Imaging (MRI), were
                      examined alongside self-reported sleep disturbances and
                      cognitive performance scores from the Alzheimer's Disease
                      Assessment Scale - Cognitive Subscale (ADAS-Cog).
                      Statistical analyses explored the effects of sleep
                      disturbances on imaging biomarkers and cognitive outcomes
                      while controlling for demographic and clinical
                      factors.ResultComparative analyses revealed that overall
                      sleep disturbances and their interaction with AD diagnosis
                      significantly impact tau deposition in key AD-sensitive
                      brain regions, including the amygdala, fusiform, inferior
                      temporal and parietal cortices, and posterior cingulate
                      cortex (corrected p-value < 0.05). These regions are
                      particularly vulnerable during the middle stages of AD.
                      Distinct patterns emerged for insomnia and SDB, with SDB
                      showing a more pronounced and earlier influence on both AD
                      pathology and cognitive decline compared to insomnia. The
                      findings suggest that SDB may be a more critical factor in
                      accelerating AD progression, emphasizing the need for early
                      intervention.ConclusionThis study demonstrates that sleep
                      disturbances significantly contribute to tau burden and
                      cognitive decline in AD, with SDB exhibiting an earlier and
                      more pronounced impact than insomnia. These findings
                      highlight the importance of targeting sleep disturbances to
                      mitigate tau-related pathology, protect cognitive function,
                      and slow disease progression. Early diagnosis and targeted
                      interventions for sleep disturbances could provide
                      significant therapeutic benefits in managing AD and
                      improving patient outcomes.},
      cin          = {INM-7},
      ddc          = {610},
      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},
      doi          = {10.1002/alz70856_099181},
      url          = {https://juser.fz-juelich.de/record/1052289},
}