The Core supports the Adult Children Study Program Project Grant by recruiting, enrolling and longitudinally following adult children, age 45-74 years at entry, of parents with and without dementia of the Alzheimer type (DAT). ACS participants age 45-64 will have clinical and psychometric assessments at entry and every 2 years thereafter (annually for ACS participants >65y). The Core is essential in that it supplies carefully characterized participants to all relevant Cores and Projects. Core data are entered by Core personnel into the database maintained by the Data Management and Biostatistics Core (DMBC). The Clinical Core interacts directly or indirectly on a daily basis with virtually every facet of the ACS PPG. The functions of the Core are to: 1. Recruit, enroll, and maintain the ACS cohort to support the Projects in this application. In the first 2 years of the grant, the Core will enroll 60 ACS participants to compensate for attrition and to bring the total sample to ~300 participants equally distributed across 3 age ranges: 45-54 years, 55-64 years, and 65-74 years. The following 3 years the Clinical Core will recruit an estimated 5 participants annually to maintain the registry of ~300 active participants. 2. Comprehensively assess the ACS participants with well-established clinical and psychometric instruments at entry and every two years (annually for participants >65 years of age). 3. Obtain blood at the initial assessment from all participants for apolipoprotein E (apoE) genotyping and banking of extracted DNA and plasma (supported by the Genetics Core of the ADRC). 4. Coordinate the participation of ACS participants in the procedures of the Biomarker Core and all Projects: (Project 1 - The natural history of Ap accumulation in preclinical AD. Project 2 - CSF markers of antecedent AD;Project 3 - Behavioral and Neural Markers of Attentional Control;Antecedents of AD;Project 4 - Antecedent Neuroimaging Biomarkers.) 5. Integrate all core data with the DMBC, and interact cooperatively with all components of the PPG. 6. Encourage the retention of ACS participants by safeguarding their research data, monitoring the participants'burden as they complete the protocols of the Cores and Projects, annually sharing with them research results, and soliciting their input into the aims and operations of the ACS.
The Clinical Core recruits, enrolls and maintains the registry of participants in the ACS study who are enrolled in 2 groups. The first group has children of a biologic parent with Alzheimer's disease (AD) and the second group has children of biologic parents who did not have AD. The objectives of this study are to identify the eariiest brain changes of AD, determine the evolution of these changes over time, and assess their predictive power for the eventual development of symptomatic AD.
|Chen, Ling; Sun, Jianguo; Xiong, Chengjie (2016) A multiple imputation approach to the analysis of clustered interval-censored failure time data with the additive hazards model. Comput Stat Data Anal 103:242-249|
|Staley, Lyndsay A; Ebbert, Mark T W; Parker, Sheradyn et al. (2016) Genome-wide association study of prolactin levels in blood plasma and cerebrospinal fluid. BMC Genomics 17 Suppl 3:436|
|Staley, Lyndsay A; Ebbert, Mark T W; Bunker, Daniel et al. (2016) Variants in ACPP are associated with cerebrospinal fluid Prostatic Acid Phosphatase levels. BMC Genomics 17 Suppl 3:439|
|Ingber, Adam P; Hassenstab, Jason; Fagan, Anne M et al. (2016) Cerebrospinal Fluid Biomarkers and Reserve Variables as Predictors of Future ""Non-Cognitive"" Outcomes of Alzheimer's Disease. J Alzheimers Dis 52:1055-64|
|Gordon, Brian A; Blazey, Tyler; Su, Yi et al. (2016) Longitudinal Î²-Amyloid Deposition and Hippocampal Volume in Preclinical Alzheimer Disease and Suspected Non-Alzheimer Disease Pathophysiology. JAMA Neurol 73:1192-1200|
|Babulal, Ganesh M; Ghoshal, Nupur; Head, Denise et al. (2016) Mood Changes in Cognitively Normal Older Adults are Linked to Alzheimer Disease Biomarker Levels. Am J Geriatr Psychiatry 24:1095-1104|
|Jack Jr, Clifford R; Knopman, David S; ChÃ©telat, GaÃ«l et al. (2016) Suspected non-Alzheimer disease pathophysiology--concept and controversy. Nat Rev Neurol 12:117-24|
|Ebbert, Mark T W; Staley, Lyndsay A; Parker, Joshua et al. (2016) Variants in CCL16 are associated with blood plasma and cerebrospinal fluid CCL16 protein levels. BMC Genomics 17 Suppl 3:437|
|Lucey, Brendan P; Mcleland, Jennifer S; Toedebusch, Cristina D et al. (2016) Comparison of a single-channel EEG sleep study to polysomnography. J Sleep Res 25:625-635|
|Cummings, Jeffrey; Aisen, Paul S; DuBois, Bruno et al. (2016) Drug development in Alzheimer's disease: the path to 2025. Alzheimers Res Ther 8:39|
Showing the most recent 10 out of 255 publications