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In contrast to the rodent model, Reference Emamian, Hall and Birnbaum33 our primate results indirectly point to a post-translational modification of striatal GSK-3β with a major shift in enzymatic activity toward its unphosphorylated (active) form in TD-expressing animals, with the potential to distinctly alter numerous targets, physiological processes, and neuroinflammation (Figure 1)

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In such a way, defined direct effect may better serve the ischemia purpose than complex procedures with L-NAME