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000275842 1001_ $$00000-0002-6561-9870$$aCorriveau-Lecavalier, Nick$$b0
000275842 245__ $$aCerebral hyperactivation across the Alzheimer's disease pathological cascade.
000275842 260__ $$a[Oxford]$$bOxford University Press$$c2024
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000275842 520__ $$aNeuronal 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.
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000275842 650_7 $$2Other$$aAlzheimer’s disease
000275842 650_7 $$2Other$$aamyloid
000275842 650_7 $$2Other$$acerebral hyperactivation
000275842 650_7 $$2Other$$afMRI
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000275842 7001_ $$00000-0002-6702-3851$$aAdams, Jenna N$$b1
000275842 7001_ $$0P:(DE-2719)9002356$$aFischer, Larissa$$b2$$udzne
000275842 7001_ $$0P:(DE-2719)9002180$$aMolloy, Eóin N.$$b3
000275842 7001_ $$0P:(DE-2719)2811815$$aMaass, Anne$$b4$$eLast author
000275842 773__ $$0PERI:(DE-600)3020013-1$$a10.1093/braincomms/fcae376$$gVol. 6, no. 6, p. fcae376$$n6$$pfcae376$$tBrain communications$$v6$$x2632-1297$$y2024
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