Fang-Chen Ma1, Yu Zong2, Hui-Fu Wang2, Jie-Qiong Li2, Xi-Peng Cao3, Lan Tan1,2. 1. Department of Neurology, Weifang Medical University, Weifang 261042, China. 2. Department of Neurology, Qingdao Municipal Hospital, Qingdao University, Qingdao 266071, China. 3. Clinical Research Center, Qingdao Municipal Hospital, Qingdao University, Qingdao 266071, China.
Abstract
BACKGROUND: ATP-binding cassette transporter A7 (ABCA7) rs3764650 has been identified to be a susceptibility locus for Alzheimer's disease (AD), but its role in cerebrospinal fluid (CSF) proteins was still unclear. METHODS: The associations of rs3764650 with CSF Aβ1-42, t-tau and p-tau were analyzed in non-dementia AD, including preclinical and prodromal AD from the Alzheimer's Disease Neuroimaging Initiative (ADNI) cohort. RESULTS: Finally, GG + GT genotypes significantly decreased CSF Aβ1-42 level, but did not alter CSF t-tau and p-tau levels in non-dementia AD at baseline, which was further confirmed in longitudinal studies. CONCLUSIONS: Our findings supported that ABCA7 modified AD risk by altering Aβ deposition rather than tau pathology.
BACKGROUND: ATP-binding cassette transporter A7 (ABCA7) rs3764650 has been identified to be a susceptibility locus for Alzheimer's disease (AD), but its role in cerebrospinal fluid (CSF) proteins was still unclear. METHODS: The associations of rs3764650 with CSF Aβ1-42, t-tau and p-tau were analyzed in non-dementia AD, including preclinical and prodromal AD from the Alzheimer's Disease Neuroimaging Initiative (ADNI) cohort. RESULTS: Finally, GG + GT genotypes significantly decreased CSF Aβ1-42 level, but did not alter CSF t-tau and p-tau levels in non-dementia AD at baseline, which was further confirmed in longitudinal studies. CONCLUSIONS: Our findings supported that ABCA7 modified AD risk by altering Aβ deposition rather than tau pathology.
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