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In exploring abnormalities associated with the syndrome, we have recently demonstrated abnormal vascular density in a FXS mouse model (Galvan and Galvez, <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"#dneu22404-bib-0015\"\/>). One of the most prominent regulators of vascular growth is VEGF\u2010A (Vascular Endothelial Growth Factor A), suggesting that FXS is associated with abnormal VEGF\u2010A expression. In addition to its role in vascular regulation, VEGF\u2010A also induces cellular changes such as increasing cell proliferation, and axonal and neurite outgrowth independent of its effects on vasculature. These VEGF\u2010A induced cellular changes are consistent with FXS abnormalities such as increased axonal material, dendritic spine density, and cell proliferation. In support of these findings, the following study demonstrated that FXS mice exhibit increased expression of VEGF\u2010A in brain. These studies suggest that increased VEGF\u2010A expression in FXS is contributing to non\u2010vascular FXS abnormalities. To explore the role of VEGF\u2010A in mediating non\u2010vascular FXS abnormalities, the monoclonal antibody Bevacizumab was used to block free VEGF\u2010A. Bevacizumab treatment was found to decrease FXS Synapsin\u20101 expression, a presynaptic marker for synapse density, and reduce FXS testicle weight to control levels. Blocking VEGF\u2010A also alleviated FXS abnormalities on novel object recognition, a test of cognitive performance. These findings demonstrate that VEGF\u2010A is elevated in FXS brain and suggest that its expression promotes non\u2010vascular FXS abnormalities. \u00a9 2016 Wiley Periodicals, Inc. Develop Neurobiol 77: 14\u201325, 2017<\/jats:p>","DOI":"10.1002\/dneu.22404","type":"journal-article","created":{"date-parts":[[2016,6,6]],"date-time":"2016-06-06T08:22:49Z","timestamp":1465201369000},"page":"14-25","source":"Crossref","is-referenced-by-count":14,"title":["Blocking elevated VEGF\u2010A attenuates non\u2010vasculature Fragile X syndrome abnormalities"],"prefix":"10.1002","volume":"77","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2029-9153","authenticated-orcid":false,"given":"Amogh P.","family":"Belagodu","sequence":"first","affiliation":[{"name":"Neuroscience Program, University of Illinois at Urbana\u2010Champaign 405 N Mathews Ave Urbana Illinois 61801"},{"name":"Beckman Institute for Advanced Science and Technology, University of Illinois at Urbana\u2010Champaign 405 N Mathews Ave Urbana Illinois 61801"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Liridon","family":"Zendeli","sequence":"additional","affiliation":[{"name":"Beckman Institute for Advanced Science and Technology, University of Illinois at Urbana\u2010Champaign 405 N Mathews Ave Urbana Illinois 61801"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bernard J.","family":"Slater","sequence":"additional","affiliation":[{"name":"Neuroscience Program, University of Illinois at Urbana\u2010Champaign 405 N Mathews Ave Urbana Illinois 61801"},{"name":"Beckman Institute for Advanced Science and Technology, University of Illinois at Urbana\u2010Champaign 405 N Mathews Ave Urbana Illinois 61801"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Roberto","family":"Galvez","sequence":"additional","affiliation":[{"name":"Neuroscience Program, University of Illinois at Urbana\u2010Champaign 405 N Mathews Ave Urbana Illinois 61801"},{"name":"Beckman Institute for Advanced Science and Technology, University of Illinois at Urbana\u2010Champaign 405 N Mathews Ave Urbana Illinois 61801"},{"name":"Psychology Department University of Illinois at Urbana\u2010Champaign 405 N Mathews Ave Urbana Illinois 61801"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2016,6,10]]},"reference":[{"key":"e_1_2_5_2_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1601-183X.2005.00128.x"},{"key":"e_1_2_5_3_1","first-page":"23","article-title":"Fmr1 knockout mice: A model to study fragile X mental retardation. 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