Eleven susceptibility loci for late-onset Alzheimer’s disease (LOAD) were identified by previous studies; however, a large portion of the genetic risk for this disease remains unexplained. We conducted a large, two-stage meta-analysis of genome-wide association studies (GWAS) in individuals of European ancestry. In stage 1, we used genotyped and imputed data (7,055,881 SNPs) to perform meta-analysis on 4 previously published GWAS data sets consisting of 17,008 Alzheimer’s disease cases and 37,154 controls. In stage 2,11,632 SNPs were genotyped and tested for association in an independent set of 8,572 Alzheimer’s disease cases and 11,312 controls. In addition to the APOE locus (encoding apolipoprotein E), 19 loci reached genome-wide significance (P < 5 × 10−8) in the combined stage 1 and stage 2 analysis, of which 11 are newly associated with Alzheimer’s disease.

Diego. ADNI data are disseminated by the Laboratory for Neuro Imaging at the University of Southern California. We thank Drs. D. Stephen Snyder and Marilyn Miller from NIA who are ex-officio ADGC members. EADI. This work has been developed and supported by the LABEX (laboratory of excellence program investment for the future) DISTALZ grant (Development of Innovative Strategies for a Transdisciplinary approach to ALZheimer's disease) including funding from MEL (Metropole européenne de Lille), ERDF (European Regional Development Fund) and Conseil Régional Rotterdam, Netherlands Organization for the Health Research and Development (ZonMw), the Research Institute for Diseases in the Elderly (RIDE), the Ministry of Education, Culture and Science, the Ministry for Health, Welfare and Sports, the European Commission (DG XII), and the Municipality of Rotterdam. The authors are grateful to the study participants, the staff from the Rotterdam Study and the participating general practitioners and pharmacists. The generation and management of GWAS genotype data for the Rotterdam Study (RS-I, RS-II, RS-III) was executed by the Human Genotyping Facility of the Genetic Laboratory of the

Objectives: To provide updated estimates of Alzheimer disease (AD) dementia prevalence in the United States from 2010 through 2050.Methods: Probabilities of AD dementia incidence were calculated from a longitudinal, populationbased study including substantial numbers of both black and white participants. Incidence probabilities for single year of age, race, and level of education were calculated using weighted logistic regression and AD dementia diagnosis from 2,577 detailed clinical evaluations of 1,913 people obtained from stratified random samples of previously disease-free individuals in a population of 10,800. These were combined with US mortality, education, and new US Census Bureau estimates of current and future population to estimate current and future numbers of people with AD dementia in the United States.Results: We estimated that in 2010, there were 4.7 million individuals aged 65 years or older with AD dementia (95% confidence interval [CI] 5 4.0-5.5). Of these, 0.7 million (95% CI 5 0.4-0.9) were between 65 and 74 years, 2.3 million were between 75 and 84 years (95% CI 5 1.7-2.9), and 1.8 million were 85 years or older (95% CI 5 1.4-2.2). The total number of people with AD dementia in 2050 is projected to be 13.8 million, with 7.0 million aged 85 years or older. Conclusion:

Brief measurement devices can alleviate respondent burden and lower refusal rates in surveys. This article reports on a field test of two shorter forms of the Center for Epidemiological Studies Depression (CES-D) symptoms index in a multisite survey of persons 65 and older. Factor analyses demonstrate that the briefer forms tap the same symptoms dimensions as does the original CES-D, and reliability statistics indicate that they sacrifice little precision. Simple transformations are presented to how scores from the briefer forms can be compared to those of the original.

The Alzheimer Disease Genetics Consortium (ADGC) performed a genome-wide association study (GWAS) of late-onset Alzheimer disease (LOAD) using a 3 stage design consisting of a discovery stage (Stage 1) and two replication stages (Stages 2 and 3). Both joint and meta-analysis analysis approaches were used. We obtained genome-wide significant results at MS4A4A [rs4938933; Stages 1+2, meta-analysis (PM) = 1.7 × 10−9, joint analysis (PJ) = 1.7 × 10−9; Stages 1–3, PM = 8.2 × 10−12], CD2AP (rs9349407; Stages 1–3, PM = 8.6 × 10−9), EPHA1 (rs11767557; Stages 1–3 PM = 6.0 × 10−10), and CD33 (rs3865444; Stages 1–3, PM = 1.6 × 10−9). We confirmed that CR1 (rs6701713; PM = 4.6×10−10, PJ = 5.2×10−11), CLU (rs1532278; PM = 8.3 × 10−8, PJ = 1.9×10−8), BIN1 (rs7561528; PM = 4.0×10−14; PJ = 5.2×10−14), and PICALM (rs561655; PM = 7.0 × 10−11, PJ = 1.0×10−10) but not EXOC3L2 are LOAD risk loci1–3.