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P4‐062: Increased p3‐Alcα, a γ‐secretase Reaction Product of Alcadein, in Plasma of Sporadic Alzheimer's Disease Subjects
Author(s) -
Konnobachelor Tomoko,
Hata Saori,
Hamada Yukiko,
Kuwano Ryozo,
Saito Yuhki,
Maeda Masahiro,
Yamamoto Takayuki,
Ihara Yasuo,
Akatsu Hiroyasu,
Suzuki. Toshiharu
Publication year - 2010
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2010.08.122
Subject(s) - biomarker , cerebrospinal fluid , disease , chemistry , medicine , biochemistry
AD and 211 cognitively normal controls (CNC). Normalized whole brain volumes (nWBV) and regional volumes of the hippocampus, parahippocampal gyrus, and entorhinal cortex were obtained in a subset of this sample (CNC n 1⁄4 154, and AD n 1⁄4 41). Results: CSF VILIP-1 levels were significantly increased in AD compared to CNC (*p < 0.0001), and strongly correlated with CSF tau (r1⁄40.70, *p < 0.0001), and p-tau181 (r1⁄40.73, *p < 0.0001), but not Ab42. CSF VILIP-1 (HR: 3.74 [95% CI: 1.98-9.58]) and VILIP-1/Ab42 (HR: 13.0 [95% CI: 4.38-30.89]) were stronger predictors of conversion from CNC to symptomatic AD than CSF tau (HR: 2.75 [95% CI: 1.31-6.97]), and tau/Ab42 (HR: 9.8 [95% CI: 3.11-21.28]), respectively. (Hazard ratios were calculated for each marker as a dichotomous variable, using the 85th percentile as a cutoff). CSF VILIP-1 showed inverse correlations with nWBV (r1⁄4-0.42, *p < 0.01), normalized volumes of the hippocampus (r1⁄4-0.61, *p 1⁄4 0<0.0001), entorhinal cortex (r1⁄4-0.48, *p < 0.004), and parahippocampal gyrus (r1⁄4-0.30, *p 1⁄4 0.03) in individuals with AD. CSF VILIP-1 was more closely related to each of these volumes than CSF tau, p-tau181, or Ab42. Conclusions: These results suggest that CSF VILIP-1 has diagnostic utility in AD and correlates closely with whole and regional brain atrophy. CSF VILIP-1/Ab42 may offer better prognostic ability than current validated CSF biomarkers (e.g. tau/Ab42) for conversion from normal cognition to cognitive impairment.