Developing an international network for Alzheimer research: The Dominantly Inherited Alzheimer Network

Abstract

The Dominantly Inherited Alzheimer Network (DIAN) is a collaborative effort of international Alzheimer disease (AD) centers that are conducting a multifaceted prospective biomarker study in individuals at-risk for autosomal dominant AD (ADAD). DIAN collects comprehensive information and tissue in accordance with standard protocols from asymptomatic and symptomatic ADAD mutation carriers and their non-carrier family members to determine the pathochronology of clinical, cognitive, neuroimaging, and fluid biomarkers of AD. This article describes the structure, implementation, and underlying principles of DIAN, as well as the demographic features of the initial DIAN cohort.

Figure 1. Administrative Structure of the Dominantly Inherited Alzheimer Network (DIAN)

Core Leaders are: JC Morris, RJ Bateman, C Xiong, NJ Cairns, AM Fagan, AM Goate, T Benzinger, and D Marcus, all of Washington University in St. Louis. Site Leaders are: RJ Bateman, JM Ringman, B Ghetti, R Mayeux, RA Sperling, S Salloway, E McDade, MN Rossor, CL Masters, RN Martins, and PR Schofield. The Alzheimer’s Disease Cooperative Study (ADCS; P Aisen, principal investigator) is the Clinical Coordinating Center for DIAN. C Jack (Mayo Clinic-Rochester) and R Koeppe (University of Michigan) provide quality review for positron imaging tomography (PET) and magnetic resonance imaging (MRI). T Foroud (Indiana University) directs the National Cell Repository for Alzheimer’s Disease (NCRAD), which maintains lymphoblast cell lines from DIAN participants. FDA: Federal Drug Administration; NIA: National Institute on Aging; ADNI: Alzheimer’s Disease Neuroimaging Initiative, Wash Univ: Washington University; UCLA: University of California Los Angeles; BWH/MGH: Brigham and Women’s Hospital/Massachusetts General Hospital.

Figure 2. Alzheimer Biomarker Pathochronology in Autosomal Dominant AD

Model derived from preliminary data presented in Bateman et al., 2012.[24] Note: The levels of CSF Aβ initially are elevated (~25y before estimated age at onset) but then are marked by progressive decline.