Objective      To elucidate the mechanism mediating the effects of apolipoprotein E (APOE for gene

apoE for protein) alleles and apoE-mimetic peptide COG1410 on early apoptosis in an

in vitro

model of experimental traumatic brain injury.       Methods      Eukaryotic expression vectors carrying individual APOE alleles (ε2

ε3

ε4) were transferred into neural stem cells (NSCs) derived from APOE knockout mice. An

in vitro

neuronal/glial co-culture model of mechanical injury was developed using a contr

olled scratch. Flow cytometry was performed to analyze the correlations among APOE genotypes

apoE-mimetic peptide COG1410 and early apoptosis.       Results      Early apoptosis after injury was observed in all groups

which was significantly higher at 24 h after injury than at 6 h and 12 h after injury (

P

<

0.05). The group transfected with APOEε4 showed more significant early apoptosis 24 h after injury as compared to the groups transfected with APOEε2 or APOEε3 (

P

<

0.05). Furthermore

decreases of early apoptosis were detected in the groups treated with apoE-mimetic peptide COG1410 at 24 h after injury (

P

<

0.01).       Conclusion      APOEε4-trasfected NSCs showing a higher rate of early apoptosis indicates that the patients with APOEε4 may suffer aggravation of brain trauma in acute stage due to early apoptosis. Our results also identify the early neuroprotective effect of apoE-mimetic peptide COG1410.