Purpose: To investigate the influence of long-chain non-coding RNA H19 on the apoptosis of Aβ treated PC12 cells and its mechanism. Methods: Exploiting Aβ treated PC12 cells to construct the Alzheimer disease (AD) model, and adopting pcDNA3.1-H19 and si-H19 plasmids to transfect PC12 cells to regulate the expression of H19. Using real-time fluorescence quantitative PCR (qRT-PCR) technology to exam the expressions of H19, miR-29b-5p, BACE1, pro-apoptotic Bax, Caspase3, and apoptosis-inhibiting gene Bcl-2 in PC12 cells. Employing Western blot (WB) to check the expressions of pro-apoptotic Bax, Caspase3, Bcl-2, BACE1 protein, and finally detecting the expression level of Aβ42 via ELISA. Results: Overexpression of H19 boosted the expressions of pro-apoptosis-related genes (i.e., Bax, Caspase3) in Aβ treated PC12 cells, while reducing the expressions of apoptosis-related genes Bcl-2; Simultaneously, miR-29b-5p expression decreased which results in the overexpression of BACE1 and Aβ 42. Inhibiting the H19 expression decreased the expressions of Bax and Caspase3 and increased the expression of Bcl-2；However, the expression of miR-29b-5p reduced which renders the expression level of BACE1 and Aβ42 decreased meaningfully. The above results are statistically significant. Conclusion: H19 participates in the regulation of AD cell model apoptosis ,which may be relevant to the miR-29b-5p/BACE1/Aβ signal pathway.