In his epoch-making monograph, Wernicke (1874) claimed that atrophy of the brain cannot cause aphasia. Refuting this claim, Pick (1892, 1898, 1901, 1904a) documented in increasing detail several cases of aphasia with circumscribed atrophy of the left temporal lobe, frontal lobe, or both, which persuaded Wernicke (1906). To explain why the atrophy is circumscribed and leads to focal symptoms, Pick (1908a) advanced a functional network account. Behavioral, neuroanatomical, and histopathological studies by Dejerine and Sérieux, Fischer, Alzheimer, Altman, Gans, Onari and Spatz, and Stertz further illuminated the clinical syndromes, the exact spatial distributions of the atrophy, the underlying disease, and its laminar specificity. Unaware of these seminal studies, research from the 1970s until now has independently rediscovered all key findings, and also supports Pick’s forgotten functional account of the distribution of atrophy and the focal symptoms. His frontal and temporal forms of aphasia foreshadowed what are now called the nonfluent/agrammatic and semantic variants of primary progressive aphasia. Moreover, aphasic symptoms may occur with frontal degeneration (what used to be called “Pick’s disease”) that yields personality changes and behavioral disturbances, now called the behavioral variant of frontotemporal dementia.