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In this study, neuronal LD accumulation was driven by tau pathology, inhibiting AMPK, an inhibitor of LD synthesis, thus increasing lipid synthesis and LD formation [49]

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Chronic effects on central A1 receptors lead to the development of the tolerance phenomenon and increased effects on A2A receptors

Furthermore, the positive association between plasma ANGPTL3 levels and incident CAD events appears to be independent of plasma lipid levels [51], suggesting that inhibiting ANGPTL3 may have a direct effect on atherosclerosis [47]

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