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Notably, several risk\u2010associated genes, such as\n                    <jats:italic>SPI1<\/jats:italic>\n                    and\n                    <jats:italic>MEF2C<\/jats:italic>\n                    , encode transcription factors (TFs) that control critical microglial functions, including phagocytosis, inflammatory responses, and neurotrophic support.\n                  <\/jats:p>\n                  <jats:p>The objective of this article is to review the recent progress in understanding these TFs and evaluate them as therapeutic targets rather than as markers of microglial state. We examine the genetic evidence implicating PU.1, MEF2C, IRF8, and BHLHE40\/41, the in vivo evidence from animal models, the transcriptional network these factors regulate, and the barriers to clinical translation.<\/jats:p>\n                  <jats:p>Because these TFs orchestrate broad gene expression networks by regulating multiple disease\u2010relevant downstream partners, targeting their expression level or activity could achieve greater therapeutic efficacy than targeting single genes, provided that the dose and disease stage of modulation are carefully considered.<\/jats:p>","DOI":"10.1002\/bies.70186","type":"journal-article","created":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T17:35:02Z","timestamp":1790703302000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Targeting Microglial Transcriptional Reprogramming as a Therapy Strategy for Alzheimer's Disease"],"prefix":"10.1002","volume":"48","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8390-7713","authenticated-orcid":false,"given":"Byungwook","family":"Kim","sequence":"first","affiliation":[{"name":"Department of Medical &amp; 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