<p>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 (<i>p</i> &lt; 0.05 and <i>p</i> &lt; 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, <i>p</i> = 0.02), whereas the CSF/plasma ratio did not differ between groups (<i>p</i> = 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.</p>

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Plasma and CSF adiponectin levels in biomarker-confirmed Alzheimer’s disease: A cross-sectional study in a tertiary memory clinic

  • Louise Sindzingre,
  • Théodore Decaix,
  • Karl Gotze,
  • Paul Baratelli,
  • Marie Bailly,
  • François Mouton-Liger,
  • Emmanuel Cognat,
  • Julien Dumurgier,
  • Agathe Vrillon,
  • Erika Cecon,
  • Claire Paquet,
  • Matthieu Lilamand,
  • Elodie Bouaziz-Amar

摘要

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.