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@ARTICLE{CorriveauLecavalier:275842,
      author       = {Corriveau-Lecavalier, Nick and Adams, Jenna N and Fischer,
                      Larissa and Molloy, Eóin N. and Maass, Anne},
      title        = {{C}erebral hyperactivation across the {A}lzheimer's disease
                      pathological cascade.},
      journal      = {Brain communications},
      volume       = {6},
      number       = {6},
      issn         = {2632-1297},
      address      = {[Oxford]},
      publisher    = {Oxford University Press},
      reportid     = {DZNE-2025-00077},
      pages        = {fcae376},
      year         = {2024},
      abstract     = {Neuronal dysfunction in specific brain regions or across
                      distributed brain networks is a known feature of Alzheimer's
                      disease. An often reported finding in the early stage of the
                      disease is the presence of increased functional MRI (fMRI)
                      blood oxygenation level-dependent signal under task
                      conditions relative to cognitively normal controls, a
                      phenomenon known as 'hyperactivation'. However, research in
                      the past decades yielded complex, sometimes conflicting
                      results. The magnitude and topology of fMRI hyperactivation
                      patterns have been found to vary across the preclinical and
                      clinical spectrum of Alzheimer's disease, including
                      concomitant 'hypoactivation' in some cases. These
                      incongruences are likely due to a range of factors,
                      including the disease stage at which the cohort is examined,
                      the brain areas or networks studied and the fMRI paradigm
                      utilized to evoke these functional abnormalities.
                      Additionally, a perennial question pertains to the nature of
                      hyperactivation in the context of Alzheimer's disease. Some
                      propose it reflects compensatory mechanisms to sustain
                      cognitive performance, while others suggest it is linked to
                      the pathological disruption of a highly regulated
                      homeostatic cycle that contributes to, or even drives,
                      disease progression. Providing a coherent narrative for
                      these empirical and conceptual discrepancies is paramount to
                      develop disease models, understand the synergy between
                      hyperactivation and the Alzheimer's disease pathological
                      cascade and tailor effective interventions. We first provide
                      a comprehensive overview of functional brain changes
                      spanning the course from normal ageing to the clinical
                      spectrum of Alzheimer's disease. We then highlight evidence
                      supporting a close relationship between fMRI hyperactivation
                      and in vivo markers of Alzheimer's pathology. We primarily
                      focus on task-based fMRI studies in humans, but also
                      consider studies using different functional imaging
                      techniques and animal models. We then discuss the potential
                      mechanisms underlying hyperactivation in the context of
                      Alzheimer's disease and provide a testable framework
                      bridging hyperactivation, ageing, cognition and the
                      Alzheimer's disease pathological cascade. We conclude with a
                      discussion of future challenges and opportunities to advance
                      our understanding of the fundamental disease mechanisms of
                      Alzheimer's disease, and the promising development of
                      therapeutic interventions incorporating or aimed at
                      hyperactivation and large-scale functional systems.},
      subtyp        = {Review Article},
      keywords     = {Alzheimer’s disease (Other) / amyloid (Other) / cerebral
                      hyperactivation (Other) / fMRI (Other) / tau (Other)},
      cin          = {AG Maaß},
      ddc          = {610},
      cid          = {I:(DE-2719)1311001},
      pnm          = {353 - Clinical and Health Care Research (POF4-353)},
      pid          = {G:(DE-HGF)POF4-353},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:39513091},
      pmc          = {pmc:PMC11542485},
      doi          = {10.1093/braincomms/fcae376},
      url          = {https://pub.dzne.de/record/275842},
}