Alzheimer disease (AD) and all other dementing illnesses are, as we never tire of telling medical and graduate students, postdoctoral fellows, and basic neuroscience colleagues, distinctly human ailments. The characteristic patterns of disintegration of the personality that characterize each of them can only be modeled in the human organism. Elegant transgenic animal models may replicate some neuropathologic features of AD, tauopathies, and many other disorders, but correlation of the pathologic brain alterations with neurobehavioral phenomena in affected animals that (with all due respect) have a fairly limited neurobehavioral repertoire becomes problematic.1- 3 Yet without doubt these important transgenic models represent a powerful approach to discovering key therapeutic targets for treating or preventing AD and related dementias—or at least manipulating genes, transcripts, and proteins within the central nervous system that we believe are of pivotal importance in AD pathogenesis.4,5 However, the decades-old exercise of clinicopathologic correlation—establishing the putative morphologic substrate(s) of a given set of signs and symptoms in a patient while she or he was alive—continues to provide extremely valuable data when both the “phenotype” of a disease and its neuropathologic correlates are carefully examined, as they have been in the elegantly simple study reported in this issue by Petersen et al.6
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