that results in increased amyloid beta levels. Results: We will report our results and discuss how they relate to the relationship between these mutations and both chemokine and amyloid beta levels in mammalian cell lines. Conclusions: This work will allow us to examine the role that amyloid beta plays in the activation of pro-in- flammatory responses by the chemokine receptors CCBP2 and CCLR2 and their respective mutants. This work could lead to a means of regulating amyloid beta production and expression which could lead to novel therapeutic solutions. P2-122 CDK5RAP2 GENE AND TAU PATHOPHYSIOLOGY IN LATE-ONSET SPORADIC ALZHEIMER’S DISEASE Justin Miron 1,2 , Cynthia Picard 1 , Jos ee Frappier 1 , Doris Dea 1 , Louise Th eroux 1 , Nathalie I. V. Nilsson 1,3 , Judes Poirier 3,4,5 , 1 Douglas Mental Health University Institute Research Centre, Montr eal, QC, Canada; 2 McGill University, Montr eal, QC, Canada; 3 McGill University, Montreal, QC, Canada; 4 Centre for the Studies on the Prevention of Alzheimer’s Disease, Douglas Mental Health University Institute, Montr eal, QC, Canada; 5 Douglas Mental Health University Institute, Montreal, QC, Canada. Contact e-mail: justin.miron@mail.mcgill.ca Background: A genome-wide association study (GWAS) was per- formed on patients with late-onset sporadic Alzheimer’s disease (AD) from the Quebec Founder Population (QFP) isolate. The most significant SNPs were validated in the French replication cohort described in Lambert et al. (2009). One of the most informa- tive polymorphisms (rs10984186) is located in the vicinity of the CDK5RAP2 locus, on chromosome 9 (OR ¼ 1.41, p ¼ 2.19 x 10 -5 ). CDK5RAP2 binds to the activator of CDK5, a kinase directly involved in Tau phosphorylation in the CNS. Methods: QFP cohort: Total RNA was purified from post-mortem human brains, reverse transcribed and processed on real-time PCR in order to measure CDK5RAP2 mRNA prevalence. CDK5RAP2 protein levels were assessed in post-mortem human brains using an ELISA assay. DNA from brain tissues was extracted using the DNeasy Tissue Kit, while DNA from blood lymphocytes was extracted from auto- mated DNA extraction. Genotyping was performed using the Illu- mina HumanHap 550k beadchip. The neuropathological staining protocol was consistent with the classification of Khachaturian. Paraffin-embedded sections were stained with modified Bielchow- sky, to observe neurofibrillary tangles. Alzheimer’s Disease Neuro- imaging Initiative (ADNI) cohort: Genotyping information was obtained via the Human 610-Quad Bead Chip. Semi-automated hippocampal volumetry assessment was carried out using the commercially available high-dimensional brain mapping tool Sur- gical Navigation Technologies. Results: CDK5RAP2 gene expres- sion levels are significantly higher in the AD group compared to aged-matched controls in the cerebellum (p < 0.001), the frontal cortex (p ¼ 0.001), and the temporal cortex (p < 0.001). Moreover, in AD subjects, CDK5RAP2 mRNA levels are significantly higher in women versus men (cerebellum: p ¼ 0.026 and temporal cortex: p ¼0.035). Furthermore, in the temporal cortex, CDK5RAP2 pro- tein levels are significantly increased in AD when compared to age-matched controls (p ¼ 0.001). In the QFP cohort, the mean density of neurofibrillary tangles correlates positively with CDK5RAP2 gene expression in the frontal cortex (p ¼ 0.021). Moreover, in the ADNI cohort, the rs10984186 variant is associated with the right hippocampal volume (p ¼ 0.00829). Conclusions: CDK5RAP2 plays an important role in the regulation and accumu- lation of Tau patholophysiology in sporadic AD. P2-123 ASSOCIATION OF CHOLESTEROL AND CHOLESTEROL METABOLISM GENES WITH COGNITIVE FUNCTION IN A POPULATION ENRICHED FOR A PARENTAL HISTORY OF ALZHEIMER’S DISEASE Karen K. Lazar 1 , Rebecca L. Koscik 2 , Leonelo E. Bautista 3 , Mark A. Sager 2 , Bruce P. Hermann 2 , Sanjay Asthana 1 , Sterling C. Johnson 1,2 , Cynthia M. Carlsson 1,2 , Corinne D. Engelman 1,3 , 1 Wisconsin Alzheimer’s Disease Research Center, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA; 2 Wisconsin Alzheimer’s Institute, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA; 3 Population Health Sciences, University of Wisconsin School of Medicine and Public Health, Madison, WI, USA. Contact e-mail: klazar@medicine.wisc.edu Background: APOE ε4 and ABCA7 variants are susceptibility genes for Alzheimer’s disease (AD). Both genes are involved in the cholesterol metabolism pathway, and mid-life cholesterol levels are associated with increased risk for AD. The interaction between APOE ε4 and ABCA7has been associated with three cognitive fac- tor scores, Verbal Learning & Memory, Working Memory, and Im- mediate Memory, in a study of participants from the Wisconsin Registry for Alzheimer’s Prevention (WRAP), a longitudinal study of middle-aged adults enriched for a parental history of AD. As a follow-up to this study, we sought to examine the influence of total serum cholesterol on this interaction effect. Methods: Linear mixed models were used to test the influence of total serum cholesterol on the APOE ε4x ABCA7effect on the three cognitive factor scores (n¼778). Each model was adjusted for age, gender, and the top two principal components of ancestry while including random ef- fects for family (siblings) and participant (repeated measures). Continuous serum cholesterol measures were included as a covar- iate where appropriate. Results: The addition of serum cholesterol to the model did not attenuate the previously reported effect of the APOE ε4x ABCA7 interaction on the three cognitive factor scores, suggesting serum cholesterol is not in the causal pathway for this association. When stratifying the population by mean total serum cholesterol, the effect of the APOE ε4x ABCA7 interaction on all three cognitive factor scores differed by tertile and AB- CA7SNP. Conclusions: Total serum cholesterol was not found to be in the causal pathway of the APOE ε4x ABCA7 interaction, but did appear to be a modifier of the interaction effect on the cogni- tive factor scores. APOE ε4 and ABCA7 genotypes along with cholesterol levels should be considered together when addressing cognitive function in at-risk populations. P2-124 THE PUERTO RICAN ALZHEIMER DISEASE INITIATIVE (PRADI): INITIAL CLINICAL FINDINGS Katrina Celis 1 , Briseida E. Feliciano-Astacio 2 , Larry Deon Adams 1 , Parker Bussies 1 , Carolina Sierra 3 , Kara L. Hamilton-Nelson 1 , Farid Rajabli 4 , Heriberto Acosta 5 , Angel Chinea 3 , Jacob L. McCauley 1 , Jeffery M. Vance 1 , Michael L. Cuccaro 1 , Gary W. Beecham 6 , Margaret A. Pericak- Vance 1 , 1 University of Miami, Miami, FL, USA; 2 Universidad Central del Caribe, Caguas, PR, Puerto Rico; 3 Universidad Central del Caribe, Bayamon, PR, Puerto Rico; 4 University of Miami Miller School of Medicine, Miami, FL, USA; 5 Clinica de la Memoria, San Juan, PR, Puerto Rico; 6 John P. Hussman Institute for Human Genomics, University of Miami Miller School of Medicine, Miami, FL, USA. Contact e-mail: kxc672@med.miami.edu Poster Presentations: Monday, July 17, 2017 P654