HIF1A and Alzheimer disease: This lack of change may be attributed to several factors: (1) Early hypoxia in AD might be compensated by alternative pathways, preventing significant fluctuations in HIF-1α levels; (2) the regulation of HIF-1α through post-translational modifications, such as acetylation, provides another layer of complexity in its stabilization (3) Differences in AD mouse models (e.g., specific mutations and disease stages examined); may influence whether or not a robust hypoxia response is triggered.