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The <jats:italic>NF1<\/jats:italic>\u2010encoded protein (neurofibromin) is an inhibitor of the oncoprotein RAS and controls cell growth and survival. Individuals with NF1 are prone to developing low\u2010grade tumors of the optic nerves, chiasm, tracts, and radiations, termed optic pathway gliomas (OPGs), which can cause vision loss. A paucity of surgical tumor specimens and of patient\u2010derived xenografts for investigative studies has limited our understanding of human NF1\u2010associated OPG (NF1\u2010OPG). However, mice genetically engineered to harbor <jats:italic>Nf1<\/jats:italic> gene mutations develop optic gliomas that share many features of their human counterparts. These genetically engineered mouse (GEM) strains have provided important insights into the cellular and molecular determinants that underlie mouse <jats:italic>Nf1<\/jats:italic> optic glioma development, maintenance, and associated vision loss, with relevance by extension to human NF1\u2010OPG disease. Herein, we review our current understanding of NF1\u2010OPG pathobiology and describe the mechanisms responsible for tumor initiation, growth, and associated vision loss in <jats:italic>Nf1<\/jats:italic> GEM models. We also discuss how <jats:italic>Nf1<\/jats:italic> GEM and other preclinical models can be deployed to identify and evaluate molecularly targeted therapies for OPG, particularly as they pertain to future strategies aimed at preventing or improving tumor\u2010associated vision loss in children with NF1.<\/jats:p>","DOI":"10.1002\/jnr.24250","type":"journal-article","created":{"date-parts":[[2018,4,28]],"date-time":"2018-04-28T13:39:59Z","timestamp":1524922799000},"page":"45-56","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":19,"title":["Insights into optic pathway glioma vision loss from mouse models of neurofibromatosis type 1"],"prefix":"10.1002","volume":"97","author":[{"given":"Morgan E.","family":"Freret","sequence":"first","affiliation":[{"name":"Department of Neurology Washington University School of Medicine St. Louis Missouri"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3127-5045","authenticated-orcid":false,"given":"David H.","family":"Gutmann","sequence":"additional","affiliation":[{"name":"Department of Neurology Washington University School of Medicine St. Louis Missouri"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2018,4,28]]},"reference":[{"key":"e_1_2_10_2_1","doi-asserted-by":"publisher","DOI":"10.3171\/jns.1988.68.1.0085"},{"key":"e_1_2_10_3_1","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/ddu389"},{"key":"e_1_2_10_4_1","doi-asserted-by":"publisher","DOI":"10.1212\/NXG.0000000000000169"},{"key":"e_1_2_10_5_1","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/ddv103"},{"key":"e_1_2_10_6_1","doi-asserted-by":"publisher","DOI":"10.3389\/fonc.2017.00251"},{"key":"e_1_2_10_7_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.ajo.2015.07.036"},{"key":"e_1_2_10_8_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.ajo.2010.08.046"},{"issue":"24","key":"e_1_2_10_9_1","first-page":"8573","article-title":"Optic nerve glioma in mice requires astrocyte Nf1 gene inactivation and Nf1 brain heterozygosity","volume":"63","author":"Bajenaru M. 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