both serum and plasma samples to determine the relationship between se- rum and plasma levels of each. We selected 11 protein biomarkers that (1) have high (greater than 0.75) expression correlation between serum and plasma; (2) are significantly associated with AD status in the TARC co- hort. We built a diagnostic algorithm with these 11 biomarkers using the TARC cohort as a training set, and validated the algorithm independently on the ADNI cohort as a testing set. Results: When the diagnostic algorithm developed on the TARC dataset and applied to the ADNI dataset, the predic- tion accuracy, sensitivity and specificity were 0.65, 0.61, and 0.74 respec- tively in distinguishing the AD patients from cognitive healthy controls. When combined with the clinical variables (age, gender, education, and APOE status), the prediction accuracy, sensitivity and specificity were 0.81, 0.84, and 0.76 respectively. Conclusions: These results validated the usefulness of the biomarkers algorithm in diagnosis of AD with both se- rum and plasma samples. The study also demonstrated by carefully select- ing appropriate protein biomarkers, it is possible to develop a diagnostic algorithm that can be applied to both serum and plasma measurements. P2-086 EVALUATION OF CSF Ab40 WITH A NEW IMMUNOASSAY INNOTEST b AMYLOID 1-40 PROTOTYPE KIT IN ALZHEIMER’S DISEASE AND APPARENTED SYNDROMES Patricia Ferrari, Laboratoire d’Homonologie - CHU de Nice, NICE, France. Background: The use of CSF Biomarkers Tau, Ptau 181 , and Aß42 as an aid in Alzheimer’s disease (AD) diagnosis is now well established in clinical routine practice in complement of imaging and clinical assessment. In about 20% of cases in our routine practice, this core biomarker panel in CSF is in- complete to conclude to AD pathology, mostly due to a discrepancy between tauopathy and amyloidopathy statements. We recently introduced in our routine practice the quantification of Aß40, which is known to reflect the to- tal amyloid load in CSF and subsequently, to permit an individual adjust- ment of the pathological amyloid Aß42 level using the Aß42/ Aß40 ratio. Innogenetics recently developed an immunoassay prototype for the quanti- fication of CSF Aß40. Our aim was to evaluate this prototype in comparison to our current routine assay for CSF Aß40 quantification (IBL Human Am- yloid (1-40) Assay kit, IBL, Japan). Methods: Innotest ß amyloid(1-40) is a solid-phase enzyme immunoassay in which the amyloid peptide is first captured by a monoclonal antibody bound on the solid phase. CSF samples are added and incubated with another biotinylated monoclonal antibody, de- tected by aperoxydase labeled streptavidin. IBL Human Amyloid (1-40) as- say is also a solid-phase sandwich ELISA using different high specific antibodies. Results: As preliminary results, 37 CSF from patients with AD, atypical profiles or normal biochemical profiles were tested for CSF Aß40 quantification, using both assays, on the same aliquots the same day. All other CSF biomarkers Tau, Ptau 181 , and Aß42 were known for all patients(using Innogenetics Innotest’s kits, Ghent, Belgium). An excellent correlation between concentration levels was found (r ¼ 0.981). The CSF Aß42/Aß40 ratios were compared and a correlation of 0.972 was found. The clinical cut-off value established at 0.05 in our routine using IBL Aß1-40 and Innotest Aß1-42 kits, was found to be at 0.0625 if Innotest Aß1-40 is used. At this cut-off ratio, the classification of CSF samples by their Aß1-42/ Aß1-40 ratios are completely concordant. Conclusions: This new Aß(1-40) assay prototype is a valuable tool to complete the current core biological marker panel to reinforce the reliability of AD pathology ev- idence in individuals. P2-087 INTEREST OF CSF P-TAU 181 AND AMYLOID- BETA 1-38 FOR THE DIAGNOSIS OF FRONTOTEMPORAL DEMENTIA Audrey Gabelle 1 , St ephane Roche 2 , Christian G eny 1 , Karim Bennys 1 , Pierre Labauge 3 , Yannick Tholance 5 , Isabelle Quadrio 5 , Laurent Tiers 2 , Baptiste Gor 2 , Chlo e Chaulet 1 , Alain Vighetto 4 , Bernard Croisile 4 , Pierre Krolak-Salmon 4 , Armand Perret-Liaudet 5 , Jacques Touchon 1 , Sylvain Lehmann 2 , 1 CHU Gui de Chauliac, CMRR Montpellier, Montpellier Cedex 5, France; 2 CHU Saint Eloi, Montpellier Cedex 5, France; 3 Centre Hospitalier Universitaire de N^ ımes, H^ opital Caremeau, N^ ımes Cedex 9, France; 4 Centre M emoire Ressources Recherche de Lyon, Lyon, France; 5 Groupement Hospitalier Est, Hospices Civils de Lyon / Universit e Claude Bernard Lyon 1, Bron Cedex, France. Background: Accurate diagnosis in dementia is becoming a requirement in order to optimize patient healthcare, caregivers’ burden and clinical trials, especially in Alzheimer disease (AD)and Fronto-Temporal Lobar Degener- ation. Recently, the scientific community revisited AD diagnosis criteria by including neuroimaging and cerebrospinal fluid (CSF) biomarkers (total and phosphorylated Tau (p-Tau), Aß42). Other CSF biomarkers like the soluble amyloid precursor protein (sAPP) a and ß isoforms, and additional Aß pep- tides (Aß38, Aß40) have been also identified as potentially interesting in de- mentia diagnosis. Methods: In this report, we present the results of the measurement of CSF Tau, p-Tau 181, Abeta38, Abeta40, Abeta42, sAPP-al- pha, and sAPP-beta in 128 patients with frontotemporal dementia (FTD, n ¼ 34), Alzheimer disease (AD, n ¼ 52) and others with neurological diseases without dementia (OND, n ¼ 42). Results: We confirmed in AD the specific increase of p-Tau and the decrease of Ab42, which are two biological hall- marks of this diagnosis. Tau concentrations were also the highest in AD and were intermediate in FTD when compared with OND. The most interesting results were obtained when focusing on amyloid biomarkers. We indeed ob- served in FTD a significant decrease of sAPPß, Aß38 and Aß40. Aß38 in particular was the best to differentiate FTD from OND. It was also very ef- ficient along with the Aß38/Aß42ratio when comparing FTD and AD. Com- bining p-Tau and Aß38 in a simple decision tree model with cut-off values at 70 ng/L and 1470 ng/L, respectively, led us for FTD detection to a high sen- sitivity of 91% and specificity at 78%. Conclusions: Finally, on a mechanis- tic point of view, the modification of amyloid biomarkers in FTD represents an additional evidence for the interrelationship between Tau and APP biol- ogy which understanding is essential to progress towards optimal therapeu- tic and diagnosis approaches of dementia. P2-088 GENOME-WIDE ASSOCIATION SCAN REPLICATION FOR BIOMARKER ENDOPHENOTYPES OF ALZHEIMER’S DISEASE Kirk Wilhelmsen 1 , Scott Chasse 1 , Nicole Griffin 1 , Ramon Diaz-Arrastia 2 , Robert Barber 3 , Donald Royall 4 , Sid O’Bryant 5 , Rachelle Doody 6 , Thomas Fairchild 7 , Roger N. Rosenberg 8 , Perrie Adams 8 , Joan Reisch 8 , 1 University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States; 2 University of Texas Southwestern Medical Center, Dallas, Texas, United States; 3 UNTHSC, Fort Worth, Texas, United States; 4 UTHSCSA Psychiatry, Fort Worth, Texas, United States; 5 Texas Tech University Health Sciences Center, Lubbock, Texas, United States; 6 Baylor College of Medicine, Houston, Texas, United States; 7 UNT Health Science Center, Fort Worth, Texas, United States; 8 UTSW Medical Center, Dallas, Texas, United States. Background: Alzheimer’s disease (AD) is the most common form of age- related dementia and one of the most serious health problems in the industrialized world. Currently available therapies provide short-term symptomatic relief, but do not slow disease progression. The development of novel therapeutic approaches requires greater knowledge of the underly- ing disease etiology. The Texas Alzheimer’s Research Consortium was cre- ated to investigate the roles of genetics, inflammation, cardiovascular disease, and metabolic disorders (e.g., hyperlipidemia, hyperinsulinemia) in AD through multi-site collaborative efforts. The ADNI project has related design characteristics that allow for replication testing of many of our GWAS conclusions with the major distinction being that a similar set of pro- teins were measured in plasma instead of serum. Methods: A genome-wide association scan (GWAS) was performed on 500 well characterized AD pa- tients and 300 cognitively normal control individuals from a longitudinal study of Alzheimer’s disease being conducted by the Texas Alzheimer’s Re- search and Care Consortium (TARCC). In addition, we analyzed serum pro- tein-based multiplex biomarker data in a subset of 197 patients diagnosed with AD and 200 controls. GWAS data were analyzed to resolve which ge- netic variants were associated with levels of the 20 proteins that were most predictive of disease status. We performed confirmatory association analysis Poster Presentations P2 S335