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Animals were exposed to a folic acid\u2010deficient diet (FAD) for 3 months and then subjected to occlusion of both common carotid arteries for 5 min. Exposure to an FAD increased plasma homocysteine levels by five\u2010 to eightfold compared with those of animals fed with a control diet (CD). In CD\u2010treated animals, most neurons were dead in the hippocampal CA1 region 4 days after ischemia\/reperfusion, whereas, in FAD\u2010treated animals, this occurred 3 days after ischemia\/reperfusion. Immunostaining for 8\u2010hydroxy\u20102\u2032\u2010deoxyguanosine (8\u2010OHdG) was performed to examine DNA damage in CA1 neurons in both groups after ischemia, and it was found that 8\u2010OHdG immunoreactivity in both FAD and CD groups peaked at 12 hr after reperfusion, although the immunoreactivity in the FAD group was much greater than that in the CD group. Platelet endothelial cell adhesion molecule\u20101 (PECAM\u20101; a final mediator of neutrophil transendothelial migration) immunoreactivity in both groups increased with time after ischemia\/reperfusion: Its immunoreactivity in the FAD group was much higher than that in the CD group 3 days after ischemia\/reperfusion. In addition, reactive gliosis in the ischemic CA1 region increased with time after ischemia in both groups, but astrocytosis and microgliosis in the FAD group were more severe than in the CD group at all times after ischemia. Our results suggest that folic acid deficiency enhances neuronal damage induced by ischemia. \u00a9 2008 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jnr.21647","type":"journal-article","created":{"date-parts":[[2008,3,11]],"date-time":"2008-03-11T19:47:47Z","timestamp":1205264867000},"page":"2003-2015","source":"Crossref","is-referenced-by-count":21,"title":["Folic acid deficiency increases delayed neuronal death, DNA damage, platelet endothelial cell adhesion molecule\u20101 immunoreactivity, and gliosis in the hippocampus after transient cerebral ischemia"],"prefix":"10.1002","volume":"86","author":[{"given":"In 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