The 43kDa transactivation response DNA-binding protein (TDP43), fused in sarcoma/translocated in liposarcoma (FUS/TLS), heat shock protein 70 (HSP70) and beta-amyloid (Aβ) are induced and involved in cerebral ischemia, amyotrophic lateral sclerosis (ALS) and Alzheimer's disease (AD), but their relationships in ischemic tolerance have never been examined where they could be involved in endogenous neuroprotection under ischemic preconditioning.Mongolian gerbils were subjected to 1 or 3 times of non-lethal 2 min-transient common carotid arteries occlusion (tCCAO). The brain samples used for Cresyl Violet staining and DAB staining of TDP43, FUS/TLS, HSP70 and Aβ.Hippocampal CA1 neurons were lost only in 2 min-3 times group at 3 and 7 days (d), which then recovered from 1 to 6 months (M). Inductions of TDP43 and FUS/TLS were accelerated from 3 M to 7 d or from 7 d to 1 d, respectively, after 2 minutes-3 times ischemia compared with 1 time. The cytoplasmic stainings of TDP43 and FUS/TLS showed a further acceleration of the peaks from 1 M to 3 d or from 1 M to 7 d, respectively, after 2 min-3 times ischemia compared with 1 time. In contrast, HSP70 was induced only at 7 d after 2 min-tCCAO for 3 times, and no expression for Aβ.In this present study, these data show that ischemic preconditioning offers a way to induce endogenous neuroprotection and neurogenesis in the gerbils, where TDP43, FUS/TLS and HSP70 are involved in this function.