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Updated: Jun 28, 2026

A High Throughput, Multiplexed and Targeted Proteomic CSF Assay to Quantify Neurodegenerative Biomarkers and Apolipoprotein E Isoforms Status
Published on: October 20, 2016
Plasma and CSF adiponectin levels in biomarker-confirmed Alzheimer's disease: A cross-sectional study in a tertiary
Louise Sindzingre1, Théodore Decaix2,3, Karl Gotze3
1Service de Gériatrie, Université Paris Cité, Institut Pasteur, AP-HP, Hôpital Lariboisière, Fondation Pour l'Audition, IHU reConnect, Paris, F-75010, France. louise.sindzingre@aphp.fr.
Abstract:
Adiponectin dysregulation has been implicated in Alzheimer's disease (AD), but the respective roles of total and high-molecular-weight (HMW) adiponectin, as well as central versus peripheral mechanisms, remain unclear. We aimed to investigate the association between biomarker-confirmed AD and plasma total adiponectin, HMW/total adiponectin ratio, and CSF/plasma adiponectin ratio, used as an indirect marker of central-peripheral distribution. We also assessed correlations with CSF amyloid and tau biomarkers. In this monocentric cross-sectional study, 134 participants (90 AD, 44 controls) from a tertiary memory clinic were included. Plasma and CSF total adiponectin were measured by ELISA, and plasma HMW adiponectin by chemiluminescent immunoassay. Associations were analyzed using multivariate linear regression adjusted for age, sex, body mass index, and APOE ε4 carriership. Plasma total and HMW adiponectin levels were higher in AD than in controls (p < 0.05 and p < 0.005, respectively), but the association was no longer significant after adjustment. The HMW/total ratio was higher in AD (0.50 vs. 0.43, p = 0.02), whereas the CSF/plasma ratio did not differ between groups (p = 0.69). No correlations were found between adiponectin (plasma total and HMW, and CSF total) and CSF amyloid or tau biomarkers. Although adiponectin levels were elevated in biomarker-confirmed AD, this association was largely driven by age, sex, and BMI. Overall, adiponectin appears to reflect systemic metabolic and nutritional status rather than AD-specific pathophysiology.
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