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Neuronal activity has a strong causal role in the production and release of the neurotoxic  β -amyloid peptide (A β ). Because of this close link, gradual accumulation of A β  into amyloid plaques has been reported in brain areas with intense neuronal activity, including cortical regions that display elevated activation at resting state. However, the link between A β  and activity is not always linear and recent studies report exceptions to the view of “more activity, more plaques.” Here, we review the literature about the activity-dependent production of A β  in both human cases and AD models and focus on the evidences that brain regions with elevated convergence of synaptic connections (herein referred to as brain nodes) are particularly vulnerable to A β  accumulation. Next, we will examine data supporting the hypothesis that, since A β  is released from synaptic terminals,  β -amyloidosis can spread in AD brain by advancing through synaptically connected regions, which makes brain nodes vulnerable to A β  accumulation. Finally, we consider possible mechanisms that account for  β -amyloidosis progression through synaptically linked regions.

Trans-Synaptic Spread of Amyloid-βin Alzheimer’s Disease: Paths toβ-Amyloidosis