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Table · dataset · 2026

Supporting data for "Adiponectin Deficiency Promotes Microglia Activation and Exacerbates Tau-Mediated Neurodegeneration"

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<p dir="ltr">Tau pathology is a pathological hallmark of neurodegenerative diseases, including Alzheimer’s disease (AD), and its progression is critically driven by microglia-mediated neuroinflammation.

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While the adipokine adiponectin (APN) exerts anti-inflammatory effects, whether it alleviates tau-mediated neurodegeneration remains unknown. In this study, we first investigated the clinical relationship between BBB-penetrant APN levels, cognitive performance, and microglial activation in cohorts of patients with AD and non-AD.

We generated a novel APN-deficient tauopathy mouse model (Tau<sup>P301S</sup>;<i>APN</i><sup><em>-/-</em></sup>) by crossbreeding APN knockout (<i>APN</i><sup><em>−/−</em></sup>) and human tau P301S mutation (Tau<sup>P301S</sup>) mice. We aimed to study: 1) whether APN deficiency recapitulates the neurodegeneration and microglial activation characteristic of tauopathies; 2) whether APN deficiency exacerbates tau-mediated neurodegeneration in Tau<sup>P301S</sup> mice; 3) whether this deficiency enhances microglia-mediated neuroinflammation in Tau<sup>P301S</sup> mice; and 4) whether pharmacological activation of the APN receptors can mitigate tau-mediated neurodegeneration by restoring microglial homeostasis.

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Animal studies included behavioural tests (open field and novel object recognition), immunofluorescent staining, Golgi staining, single-nucleus RNA sequencing, and ELISA. In vitro studies included microglial phagocytosis, lysosomal activity, and MTT assay.</p>

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Disease 75% · RNA sequencing 75% · Sequencing 75%
Provenance · 1 source records, 20 field assertions
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