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Alzheimer disease

From inherited to sporadic AD—crossing the biomarker bridge

Whether dominantly inherited variants of Alzheimer disease (AD) and 'sporadic' forms exhibit similar pathophysiological and biomarker signatures remains unresolved. A landmark study has proposed a biomarker progression model of dominantly inherited AD, but a complex systems biology and physiology approach is required to translate these findings to sporadic disease.

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Figure 1: The genetic and research paradigms of familial AD and sporadic AD.

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Correspondence to Harald Hampel.

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Competing interests

H. Hampel has received lecture honoraria and/or research grants and/or travel funding and/or participated in scientific advisory boards of the following pharmaceutical companies that are involved in the manufacture and marketing of diagnostics and/or drugs or medicinal products for Alzheimer disease: Astra-Zeneca, Avid, Bayer, BMS, Boehringer-Ingelheim, Eisai, Elan, Eli Lilly, GE Healthcare, Genentech, GlaxoSmithKline Bio, Janssen-Cilag, Merz Pharmaceuticals, Novartis, Pfizer, Sanofi-Aventis, Schwabe, Roche, and Wyeth. S. Lista declares no competing interests.

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Hampel, H., Lista, S. From inherited to sporadic AD—crossing the biomarker bridge. Nat Rev Neurol 8, 598–600 (2012). https://doi.org/10.1038/nrneurol.2012.202

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