A tiny piece of the protein thymosin‑beta‑4, called Ac‑SDKP, was directly injected into the brains of mice and was found to boost the creation of new hippocampal neurons and improve their ability to navigate mazes. The study shows a possible brain‑health benefit, but the way it was given (direct brain infusion) isn’t something you can easily do at home, and human data are missing.

Although several studies have suggested the neuroprotective effect of thymosin β4 (TB4), a major actin-sequestering protein, on the central nervous system, little is understood regarding the action of N-acetyl-serylaspartyl-lysyl-proline (Ac-SDKP), a peptide fragment of TB4 on brain function. Here, we examined neurogenesis-stimulative effect of Ac-SDKP. Intrahippocampal infusion of Ac-SDKP facilitated the generation of new neurons in the hippocampus. Ac-SDKP-treated mouse hippocampus showed an increase in β-catenin stability with reduction of glycogen synthase kinase-3β (GSK-3β) activity. Moreover, inhibition of vascular endothelial growth factor (VEGF) signaling blocked Ac-SDKP-facilitated neural proliferation. Subchronic intrahippocampal infusion of Ac-SDKP also increased spatial memory. Taken together, these data demonstrate that Ac-SDKP functions as a regulator of neural proliferation and indicate that Ac-SDKP may be a therapeutic candidate for diseases characterized by neuronal loss.