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These interactions stabilize the inactive conformation of GSK3βΞ², preventing its hyperactivity, which is associated with tau hyperphosphorylation and neurofibrillary tangle formation (Figure 5aβh)
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In primary microglial cells, INM-176 significantly inhibited LPS-induced nitric oxide release and expression of tumor necrosis factor-Ξ± and interleukin-1Ξ²
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