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        <identifier>oai:figshare.com:article/33228621</identifier>
        <datestamp>2026-09-21T01:38:59Z</datestamp>
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          <dc:title>Supporting data for "Adiponectin Deficiency Promotes Microglia Activation and Exacerbates Tau-Mediated Neurodegeneration"</dc:title>
          <dc:creator>Zifei Zhang (12989555)</dc:creator>
          <dc:subject>Central nervous system</dc:subject>
          <dc:subject>Alzheimer's disease</dc:subject>
          <dc:subject>Neurodegeneration</dc:subject>
          <dc:subject>Tauopathies</dc:subject>
          <dc:subject>Microglia</dc:subject>
          <dc:subject>Neuroinflammation</dc:subject>
          <dc:subject>Adiponectin</dc:subject>
          <dc:description>&lt;p dir="ltr"&gt;Tau pathology is a pathological hallmark of neurodegenerative diseases, including Alzheimer’s disease (AD), and its progression is critically driven by microglia-mediated neuroinflammation. 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&lt;sup&gt;P301S&lt;/sup&gt;;&lt;i&gt;APN&lt;/i&gt;&lt;sup&gt;&lt;em&gt;-/-&lt;/em&gt;&lt;/sup&gt;) by crossbreeding APN knockout (&lt;i&gt;APN&lt;/i&gt;&lt;sup&gt;&lt;em&gt;−/−&lt;/em&gt;&lt;/sup&gt;) and human tau P301S mutation (Tau&lt;sup&gt;P301S&lt;/sup&gt;) 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&lt;sup&gt;P301S&lt;/sup&gt; mice; 3) whether this deficiency enhances microglia-mediated neuroinflammation in Tau&lt;sup&gt;P301S&lt;/sup&gt; mice; and 4) whether pharmacological activation of the APN receptors can mitigate tau-mediated neurodegeneration by restoring microglial homeostasis. 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.&lt;/p&gt;</dc:description>
          <dc:date>2026-09-21T01:38:59Z</dc:date>
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          <dc:identifier>10.25442/hku.33228621.v1</dc:identifier>
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          <dc:rights>CC BY-NC 4.0</dc:rights>
          <dc:rights>Embargoed</dc:rights>
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