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Frozen and paraffin-embedded tissue samples resected from superior temporal lobes of 92 patients undergoing temporal lobectomies as a treatment for medication-resistant temporal lobe epilepsy were used in this study. To determine if epilepsy-related changes reflect those in another neurological condition, analogous tissue samples harvested from 10 autopsy-verified Alzheimer brains, and from 10 neurologically and neuropathologically normal control patients were analyzed using immunofluorescence histochemistry, western immunoblot, and real-time PCR to determine genotype effects on neuronal number and size, neuronal and glial expressions of amyloid \u03b2 (A\u03b2) precursor protein (\u03b2APP), A\u03b2, apolipoprotein E (ApoE), S100B, interleukin-1\u03b1 and \u03b2, and \u03b1 and \u03b2 secretases; and on markers of neuronal stress, including DNA\/RNA damage and caspase 3 expression.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Results<\/jats:title>\n            <jats:p>Allelic combinations of <jats:italic>APOE<\/jats:italic> influenced each epilepsy-related neuronal and glial response measured as well as neuropathological change. <jats:italic>APOE<\/jats:italic> \u03f53,3 conferred greatest neuronal resilience denoted as greatest production of the acute phase proteins and low neuronal stress as assessed by DNA\/RNA damage and caspase-3 expression. Among patients having an <jats:italic>APOE<\/jats:italic> \u03f52 allele, none had A\u03b2 plaques; their neuronal sizes, like those with <jats:italic>APOE<\/jats:italic> \u03f53,3 genotype were larger than those with other genotypes. <jats:italic>APOE<\/jats:italic> \u03f54,4 conferred the weakest neuronal resilience in epilepsy as well as in Alzheimer patients, but there were no <jats:italic>APOE<\/jats:italic> genotype-dependent differences in these parameters in neurologically normal patients.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p>Our findings provide evidence that the strength of the neuronal stress response is more related to patient <jats:italic>APOE<\/jats:italic> genotype than to either the etiology of the stress or to the age of the patient, suggesting that <jats:italic>APOE<\/jats:italic> genotyping may be a useful tool in treatment decisions.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1186\/2051-5960-1-41","type":"journal-article","created":{"date-parts":[[2013,7,29]],"date-time":"2013-07-29T12:14:29Z","timestamp":1375100069000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":32,"title":["Epilepsy: neuroinflammation, neurodegeneration, and APOE genotype"],"prefix":"10.1186","volume":"1","author":[{"given":"Orwa","family":"Aboud","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert E","family":"Mrak","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Frederick A","family":"Boop","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"W Sue T","family":"Griffin","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2013,7,29]]},"reference":[{"key":"38_CR1","doi-asserted-by":"publisher","first-page":"754","DOI":"10.1212\/WNL.0b013e31828250c5","volume":"80","author":"JH Chin","year":"2013","unstructured":"Chin JH: The global fund for epilepsy: a proposal. 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