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Hypothetical model of accumulating late-onset Alzheimer’s disease (AD) pathophysiology, including Aβ deposition, synaptic dysfunction, tauopathy-associated neuronal injury, volumetric reductions, and cognitive and functional declines. Dashed lines indicate that synaptic dysfunction may be detectable before Aβ accumulation in carriers of the ε4 allele of the apolipoprotein E. Figure is reprinted with permission from Sperling et al., 2011
