{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T20:26:14Z","timestamp":1791923174599,"version":"4.3.4"},"reference-count":55,"publisher":"MDPI AG","issue":"19","license":[{"start":{"date-parts":[[2025,10,8]],"date-time":"2025-10-08T00:00:00Z","timestamp":1759881600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"Cecil H. and Ida Green Distinguished Chair fund"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["IJMS"],"abstract":"<jats:p>The deposition of amyloid beta (A\u03b2) in the human brain is a hallmark of Alzheimer\u2019s disease (AD). A\u03b2 has been shown to exert a wide range of effects on neurons in cell and animal models. Here, we take advantage of differentiated neurons from iPSC-derived neural stem cells of human donors to examine its effects on human neurons. Specifically, we employed two types of neurons from genetically distinct donors: one male carrying APO E2\/E2 (M E2\/E2) and one female carrying APO E3\/E3 (F E3\/E3). Genome-wide RNA-sequencing analysis identified 64 and 44 genes that were induced by A\u03b2 in M E2\/E2 and F E3\/E3 neurons, respectively. GO and pathway analyses showed that A\u03b2-induced genes in F E3\/E3 neurons do not constitute any statistically significant pathways whereas A\u03b2-induced genes in M E2\/E2 neurons constitute a complex network of activated pathways. These pathways include those promoting inflammatory responses, such as IL1\u03b2, IL4, and TNF, and those promoting cell migration and movement, such as chemotaxis, migration of cells, and cell movement. These results strongly suggest that the effects of A\u03b2 on neurons are highly dependent on their genetic background and that A\u03b2 can promote strong responses in inflammation and cell migration in some, but not all, neurons.<\/jats:p>","DOI":"10.3390\/ijms26199804","type":"journal-article","created":{"date-parts":[[2025,10,9]],"date-time":"2025-10-09T09:41:02Z","timestamp":1760002862000},"page":"9804","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Preexisting Genetic Background Primes the Responses of Human Neurons to Amyloid \u03b2"],"prefix":"10.3390","volume":"26","author":[{"ORCID":"https:\/\/orcid.org\/0009-0006-2052-7696","authenticated-orcid":false,"given":"Adedamola Saidi","family":"Soladogun","sequence":"first","affiliation":[{"name":"Department of Biological Sciences, The University of Texas at Dallas, 800 W Campbell Rd, Mail Stop RL11, Richardson, TX 75080, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9242-0763","authenticated-orcid":false,"given":"Li","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Biological Sciences, The University of Texas at Dallas, 800 W Campbell Rd, Mail Stop RL11, Richardson, TX 75080, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2025,10,8]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","unstructured":"Alzheimer\u2019s Association (2024). 2024 Alzheimer\u2019s Disease Facts and Figures. 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