Higher Plasma APOC-III Was Associated with a Slower Reduction of β-Amyloid Levels in Cerebrospinal Fluid Among Older Individuals Without Dementia
Xiaoyan Zhang On behalf of the Alzheimer’s Disease Neuroimaging Initiative
Department of Child Healthcare, The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University, Wenzhou, People’s Republic of China
Correspondence: Xiaoyan Zhang
The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University, 109 Xueyuan West Road, Wenzhou 325027, Zhejiang Province, People’s Republic of China
Purpose: Although emerging evidence has suggested that apolipoprotein C-III (APOC-III) is involved in the pathogenesis of Alzheimer’s disease (AD), the association of APOC-III with longitudinal changes in cerebrospinal fluid (CSF) AD pathologies (β-amyloid (Aβ 42) and tau proteins) is not clear. In the present study, we aimed to examine whether plasma APOC-III levels are associated with longitudinal changes in CSF Aβ 42, total-tau (t-tau), and phosphorylated-tau (p-tau) levels among older individuals without dementia.
Patients and Methods: Linear mixed models were fitted with plasma APOC-III used as a predictor for longitudinal changes in CSF AD biomarkers over a 7-year period. Data were obtained from the Alzheimer’s Disease Neuroimaging Initiative database, and 195 older individuals without dementia (47 subjects with normal cognition (NC) and 148 subjects with mild cognitive impairment (MCI)) with baseline plasma APOC-III measurements were included.
Results: Among older individuals without dementia, we found that the tertiles of plasma APOC-III were associated with changes in CSF Aβ 42, but not t-tau or p-tau. Specifically, the CSF Aβ 42 reduction for individuals in the highest plasma APOC-III tertile was significantly slower compared with those in the middle tertile, whereas no other pairwise difference was found to be statistically significant.
Conclusion: Among older individuals without dementia, higher plasma APOC-III levels were associated with slower declines in CSF Aβ 42.
Keywords: Alzheimer’s disease, apolipoprotein C-III, beta-amyloid, tau proteins, longitudinal study
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