Minjung Wang

COMPARISON BETWEEN THE MINI-MENTAL STATE EXAMINATION AND THE MINI-MENTAL STATE EXAMINATION-2 IN KOREAN PATIENTS WITH MILD COGNITIVE IMPAIRMENT AND ALZHEIMER’S DISEASE

over time. Even among those (n1⁄4282) we have previously identified as ‘false positive’ MCI diagnostic errors in ADNI (Edmonds et al., 2015), only 15 of the 24 ADNI reverters were baseline ‘false positives’, thereby missing 94.7% of participants in whom a cognitively normal diagnosis appears better justified based on neuropsychological performance, normal biomarkers, lack of cortical thinning, and low progression rates. Additionally, compared to ADNI, the NP criteria identified more new MCI cases and greater CSF reductions in b-amyloid in normal-to-MCI individuals, consistent with their cognitive decline. We conclude that ADNI has an artificially low reversion rate (3%) even when compared to metaanalytic reversion rates (24%) based largely on conventional criteria (Malek-Ahmadi, 2016).

AMYLOID BETA OLIGOMERIZATION IN PLASMA AS A POTENTIAL BLOOD-BASED BIOMARKER FOR ALZHEIMER’S DISEASE

Model 1 Per g/dL increase (n1⁄4233) 0.11(0.03,0.18) -0.11 (-0.18, -0.04) -0.12 (-0.18, -0.05) >14 g/dL (n1⁄475) Reference Reference Reference 12-14 g/dL (n1⁄484) 0.18 (-0.11,0.48) -0.05 (-0.33, 0.23) 0.10 (-0.17, 0.37) <12 g/dL (n1⁄474) -0.34 (-0.65, -0.02) 0.32 (0.03, 0.61) 0.36 (0.08, 0.64) P for trend 0.038 0.031 0.013 Model 2 Per g/dL increase (n1⁄4233) 0.11(0.03,0.19) -0.11 (-0.19, -0.04) -0.08 (-0.14, -0.01) >14 g/dL (n1⁄475) Reference Reference Reference 12-14 g/dL (n1⁄484) 0.14 (-0.16,0.44) -0.02 (-0.30, 0.26) 0.09 (-0.18, 0.37) <12 g/dL (n1⁄474) -0.68 (-0.59, -0.01) 0.30 (-0.01,0.62) 0.21 (-0.08, 0.52) P for trend 0.064 0.067 0.163

NOVEL AND KNOWN RARE SORL1 MUTATIONS IN KOREAN AD PATIENTS

Figure 2. Comparison of tau SUVR levels in cognitively unimpaired (Unimp) HIV+ vs. cognitively impaired (lmp) HIV+ subjects. Levels are shown in the entorhinal, inferior temporal (inftemp), medial orbitofrontal (medorbfrntl) and anterior cingulate (ant cc) cortex, and in the precuneus and insula. Figure 3. Comparison of tau SUVR levels in entorhinal cortex plotted against nadir CD4 cell count for HIV+ subjects (N1⁄417). The p-value for a linear relationship is 0.57. Poster Presentations: Tuesday, July 18, 2017 P965

NOVEL, PSEN1 T119I MUTATION IN AN EARLY-ONSET ALZHEIMER'S DISEASE PATIENT

Eva Bagyinszky, Vo Van Giau, Young Ho Park, Minjung Wang, So Young Park, Jae Won Jang, Young Chul Youn, Seong Soo An, SangYun Kim, Gachon University, Seongnam, South Korea; Gachon University, Seongnam, South Korea; Clinical Neuroscience Center, Seoul National University Bundang Hospital, Seongnam, Republic of Korea; 4 Clinical Neuroscience Center, Seoul National University Bundang Hospital, Seongnam, South Korea; 5 Kangwon National University, Chuncheon, Republic of Korea; Chung-Ang University Hospital, Seoul, South Korea; Seoul National University Bundang Hospital, Seongnam, South Korea; 8 Seoul National University Bundang Hospital, Seongnam, Republic of Korea. Contact e-mail: navigator120@gmail.com

Genetics of early-onset Alzheimer’s disease (AD) in korea: An update

the Assessment of Neuropsychological Status (RBANS) was also evaluated for the PREVENT-AD cohort. Results: In the QFP, the 299Gly allele was present in 6.3% of LOAD cases and 10.7% of aged-matched control subjects (p 0.005). Healthy subjects enrolled in the PREVENT-AD study (with a first-degree family history of AD) were positive for the 299Gly allele in a proportion of 12.5%. In ADNI, the 299Gly allele was detected in 9.5% of AD cases, 9.9% ofMCI patients and 11.2% of control subjects (baseline diagnostic, p 0.05). Although not associated with the disease in the latter population, the 299Gly allele significantly correlated with higher CSF APOE levels measured in MCI patients. In unaffected subjects from the PREVENT-AD cohort, the 299Gly allele was significantly associated with enhanced cortical thickness and a higher RBANS visuospatial score. Conclusions: The presence of the 299Gly allele is clearly associated with neuroprotection. Targeting TLR4 signaling pathway could be considered for pharmacological intervention to prevent Alzheimer’s disease.