The scientific objective of establishing an international network for identification, evaluation, and longitudinal follow-up of families with early onset dominantly inherited Alzheimer's disease (AD) is addressed in the overview of this renewal application and in Core B: Clinical. The activities of the Core C: Biostatistics are designed to enhance the research objectives of DIAN by serving the DIAN investigators with a smooth transition from the database to statistical analyses, providing appropriate statistical analysis resources to all Cores, and developing necessary longitudinal statistical models to test the preclinical hypotheses of DIAN on all major biomarkers of AD. The major hypotheses in DIAN conjecture a period of preclinical AD in individuals who are destined to develop early onset dementia (mutation carriers) that can be detected by changes in biological fluids and in neuroimaging correlates in comparison with individuals who will not develop early onset dementia (noncarriers) and a temporal difference in preclinical changes across these correlates for mutation carriers. The methodological significance of the hypothesis is the requirement of state-of-the-art longitudinal statistical models to adequately estimate and compare the longitudinal rates of change on multi-modal disease markers during the preclinical period, and to assess their association with the risk of subsequent development of symptomatic AD.
In the proposed DIAN renewal, Core C: Biostatistics Core will bridge the transition from the DIAN database stored and managed by Core H: Informatics Core to the analyses of the longitudinal as well as cross-sectional data. Specifically, the Biostatistics Core will oversee the statistical quality control of data and appropriate data analyses for the study by producing appropriately de-identified and statistically analyzable datasets for distribution/analysis and leading the statistical data analyses for all Cores.
|Stout, Sarah H; Babulal, Ganesh M; Ma, Chunyu et al. (2018) Driving cessation over a 24-year period: Dementia severity and cerebrospinal fluid biomarkers. Alzheimers Dement 14:610-616|
|Villeneuve, Sylvia; Vogel, Jacob W; Gonneaud, Julie et al. (2018) Proximity to Parental Symptom Onset and Amyloid-? Burden in Sporadic Alzheimer Disease. JAMA Neurol 75:608-619|
|Lim, Yen Ying; Hassenstab, Jason; Goate, Alison et al. (2018) Effect of BDNFVal66Met on disease markers in dominantly inherited Alzheimer's disease. Ann Neurol 84:424-435|
|Suárez-Calvet, Marc; Capell, Anja; Araque Caballero, Miguel Ángel et al. (2018) CSF progranulin increases in the course of Alzheimer's disease and is associated with sTREM2, neurodegeneration and cognitive decline. EMBO Mol Med 10:|
|Besser, Lilah; Kukull, Walter; Knopman, David S et al. (2018) Version 3 of the National Alzheimer's Coordinating Center's Uniform Data Set. Alzheimer Dis Assoc Disord 32:351-358|
|Kinnunen, Kirsi M; Cash, David M; Poole, Teresa et al. (2018) Presymptomatic atrophy in autosomal dominant Alzheimer's disease: A serial magnetic resonance imaging study. Alzheimers Dement 14:43-53|
|Lee, Seonjoo; Zimmerman, Molly E; Narkhede, Atul et al. (2018) White matter hyperintensities and the mediating role of cerebral amyloid angiopathy in dominantly-inherited Alzheimer's disease. PLoS One 13:e0195838|
|Xiong, Chengjie; Luo, Jingqin; Chen, Ling et al. (2018) Estimating diagnostic accuracy for clustered ordinal diagnostic groups in the three-class case-Application to the early diagnosis of Alzheimer disease. Stat Methods Med Res 27:701-714|
|Karch, Celeste M; Hernández, Damián; Wang, Jen-Chyong et al. (2018) Human fibroblast and stem cell resource from the Dominantly Inherited Alzheimer Network. Alzheimers Res Ther 10:69|
|Day, Gregory S; Gordon, Brian A; Perrin, Richard J et al. (2018) In vivo [18F]-AV-1451 tau-PET imaging in sporadic Creutzfeldt-Jakob disease. Neurology 90:e896-e906|
Showing the most recent 10 out of 59 publications