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The default mode network (DMN) is a unique idea that attracts many neuroimaging researchers to examine alterations in the resting-state brain physiology in normal aging and psychiatric and neurological disorders predominantly by using functional magnetic resonance imaging (fMRI). In dementias, especially in Alzheimer’s disease (AD), one of the recent topics in an imaging domain is depicting its pathological substance, β-amyloid protein (Aβ)  in vivo  using positron emission tomography (PET). This Aβ accumulation was not only discovered in AD but also frequently in cognitively normal people. Indeed, there is evidence that subjects with high Aβ deposition tend to be considered as those who are very likely to develop AD in the future. Recent reports also show that the DMN in AD patients is affected in conjunction with Aβ deposition. Our recent study of the cognitive and physiological impact of Aβ accumulation on the DMN function in normal elderly people using PET has shown that the amount of Aβ deposits is negatively correlated with the DMN function, and the lower function of the DMN is associated with poorer working memory performance. As expected, Aβ deposition in the brain, however minute the degree of its accumulation can be, may cause neuronal discoordination in the DMN along with poor working memory in normal aging. As literature on fMRI-based DMN activity is profuse, here, we discuss the pathophysiological aspect of the DMN from a molecular imaging viewpoint.

A review of the default mode network in aging and dementia based on molecular imaging