N-acetyl-serylaspartyl-lysyl-proline (Ac-SDKP), a peptide fragment of thymosin β4 facilitated hippocampal neurogenesis.
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Ac-SDKP increase in β-catenin stability with reduction of glycogen synthase kinase-3β activity.
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Moreover, inhibition of VEGF signaling blocked Ac-SDKP-facilitated neural proliferation.
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Subchronic intrahippocampal infusion of Ac-SDKP also increased spatial memory.
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Taken together, these data demonstrate that TB4 functions as a regulator of neurogenesis.
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