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A unique window into this reorganization is provided by presymptomatic cases of familial Alzheimer's disease (FAD). Here we studied neural circuitry related to semantic processing in presymptomatic FAD cases by estimating the intracranial sources of the N400 event\u2010related potential (ERP). ERPs were obtained during a semantic\u2010matching task from 24 presymptomatic carriers and 25 symptomatic carriers of the E280A presenilin\u20101 (<jats:italic>PS\u20101<\/jats:italic>) mutation, as well as 27 noncarriers (from the same families). As expected, the symptomatic\u2010carrier group performed worse in the matching task and had lower N400 amplitudes than both asymptomatic groups, which did not differ from each other on these variables. However, N400 topography differed in mutation carrier groups with respect to the noncarriers. Intracranial source analysis evinced that the presymptomatic\u2010carriers presented a decrease of N400 generator strength in right inferior\u2010temporal and medial cingulate areas and increased generator strength in the left hippocampus and parahippocampus compared to the controls. This represents alterations in neural function without translation into behavioral impairments. Compared to controls, the symptomatic\u2010carriers presented a similar anatomical shift in the distribution of N400 generators to that found in presymptomatic\u2010carriers, albeit with a larger reduction in generator strength. The redistribution of N400 generators in presymptomatic\u2010carriers indicates that early focal degeneration associated with the mutation induces neural reorganization, possibly contributing to a functional compensation that enables normal performance in the semantic task. 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