GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE268nnn/GSE268702/primaryOK200TranscriptomicsMus musculusExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE268702GEOGSEfalseEffect of MEIS2 overexpression on HT22 cellsWe determined MEIS2 was notably elevated in AD models and AD patients. Alterations in the expression of MEIS2 can modulate the levels of BACE1. MEIS2 down-regulation improved the learning and memory retention of AD mice and decreased the number of amyloid plaques. MEIS2 binds to the BACE1 promoter, positively regulates BACE1 expression, and accelerates APP amyloid degradation in vitro. Therefore, our findings suggest that MEIS2 might be a critical transcription factor in AD, since it regulates BACE1 expression and accelerates BACE1-mediated APP amyloidogenic cleavage. MEIS2 is a promising early intervention target for AD treatment.2026/05/29GSE268702GSM8297152GSM8297151GSM8297150GSM829714934290268702Mus musculus