{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T01:27:50Z","timestamp":1790731670283,"version":"4.1.0"},"reference-count":10,"publisher":"SAGE Publications","issue":"4","license":[{"start":{"date-parts":[[2025,4,16]],"date-time":"2025-04-16T00:00:00Z","timestamp":1744761600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"},{"start":{"date-parts":[[2025,4,16]],"date-time":"2025-04-16T00:00:00Z","timestamp":1744761600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Epilepsy Curr"],"published-print":{"date-parts":[[2025,8]]},"abstract":"<jats:p>\n                    <jats:boxed-text orientation=\"portrait\" position=\"float\">\n                      <jats:p>\n                        <jats:bold>Progression of Amyloid Accumulation in Late Adulthood Among People With Childhood-Onset Epilepsy.<\/jats:bold>\n                      <\/jats:p>\n                      <jats:p>\n                        Joutsa J, Rinne JO, Niemi KJ, Karrasch M, Parkkola RK, Saunavaara J, Helin SP, Hermann BP, Sillanp\u00e4\u00e4 M. Neurology. 2025;104(3):e210303. doi:\n                        <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"uri\" xlink:href=\"https:\/\/doi.org\/10.1212\/WNL.0000000000210303\">10.1212\/WNL.0000000000210303<\/jats:ext-link>\n                        .\n                      <\/jats:p>\n                      <jats:p>\n                        Background and objectives: Previous research has demonstrated increased brain amyloid plaque load in individuals with childhood-onset epilepsy in late middle age. However, the trajectory of this process is not yet known. The aim of this study was to determine whether individuals with a history of childhood-onset epilepsy show progressive brain aging in amyloid accumulation in late adulthood (Turku Adult Childhood-Onset Epilepsy study, TACOE). Methods: Adults from a prospective population-based cohort of individuals with childhood-onset epilepsy, originally recruited 1961-1964, together with matched controls, were scanned with [\n                        <jats:sup>11<\/jats:sup>\n                        C]PIB PET twice: after at least 50 years (TACOE-50) and again after at least 55 years (TACOE-55) from the diagnosis. Results: At TACOE-55, 31.4% (11\/36, mean age 63.3 years, 52.8% female) of individuals from the epilepsy group and 11.4% (4\/35, 63.1 year, 54.3%) of controls had a visually abnormal [\n                        <jats:sup>11<\/jats:sup>\n                        C]PIB scan (\n                        <jats:italic toggle=\"yes\">p<\/jats:italic>\n                        = 0.039). At TACOE-55, cortical brain [\n                        <jats:sup>11<\/jats:sup>\n                        C]PIB uptakes were higher and increased more from TACOE-50 in the epilepsy compared with the control group (\n                        <jats:italic toggle=\"yes\">p<\/jats:italic>\n                        &lt; 0.05). In voxelwise whole-brain analyses, the epilepsy group showed significantly higher and more widespread brain amyloid accumulation (\n                        <jats:italic toggle=\"yes\">p<\/jats:italic>\n                        <jats:sub>FWE<\/jats:sub>\n                        &lt; 0.05). Discussion: The results demonstrate that childhood-onset epilepsy is associated with an earlier age at onset of amyloidosis and greater progressive amyloid accumulation in late adulthood.\n                      <\/jats:p>\n                      <jats:p>\n                        <jats:bold>Amyloid deposition in adults with drug-resistant temporal lobe epilepsy<\/jats:bold>\n                      <\/jats:p>\n                      <jats:p>\n                        Fonseca E, Lallana S, Ortega G, Cano A, Sarria-Estrada S, Pareto D, Quintana M, Lorenzo-Bosquet C, L\u00f3pez-Maza S, Gifreu A, Campos-Fern\u00e1ndez D, Abraira L, Santamarina E, Orellana A, Montrreal L, Puerta R, Aguilera N, Ramis M, de Rojas I, Ruiz A, T\u00e1rraga L, Rovira \u00c0, Marqui\u00e9 M, Boada M, Toledo M. Epilepsia. 2024 Dec;65(12):3664\u20133675. doi:\n                        <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"uri\" xlink:href=\"https:\/\/doi.org\/10.1111\/epi.18142\">10.1111\/epi.18142<\/jats:ext-link>\n                        .\n                      <\/jats:p>\n                      <jats:p>\n                        Objective: Pathological amyloid-\u03b2 (A\u03b2) accumulation and hyperphosphorylated tau proteins have been described in resected temporal lobe specimens of epilepsy patients. We aimed to determine cerebrospinal fluid (CSF) A\u03b21\u201342 and p181-tau levels and cerebral A\u03b2 deposits on positron emission tomography (A\u03b2 PET) and correlate these findings with cognitive performance in adults with drug-resistant temporal lobe epilepsy (TLE). Methods: In this cross-sectional study, we enrolled individuals with drug-resistant TLE who were 25\u201355 years old. Each participant underwent\n                        <jats:sup>18<\/jats:sup>\n                        F-flutemetamol PET, determination of CSF A\u03b21\u201342, p181-tau, and total tau, and a comprehensive neuropsychological assessment. We evaluated normalized standard uptake value ratios (SUVRs) for different brain regions on A\u03b2 PET. Results: Thirty patients (mean age\u2009=\u200941.9\u2009\u00b1\u2009SD 8.1 years, 57% men) were included. The median disease duration was 9.5 (interquartile range\u2009=\u20094\u201324) years. Twenty-six patients (87%) had a clinically significant cognitive impairment on neuropsychological evaluation, 18 (69%) of the amnesic type. On A\u03b2 PET, high uptake was observed in both mesial temporal regions (ipsilateral: SUVR\n                        <jats:italic toggle=\"yes\">z<\/jats:italic>\n                        -score\u2009=\u2009.90, 95% confidence interval [CI]\u2009=\u2009.60\u20131.20; contralateral: SUVR\n                        <jats:italic toggle=\"yes\">z<\/jats:italic>\n                        -score\u2009=\u2009.92, 95% CI\u2009=\u2009.57\u20131.27;\n                        <jats:italic toggle=\"yes\">p<\/jats:italic>\n                        \u2009&lt;\u2009.001), which was higher when compared to SUVR\n                        <jats:italic toggle=\"yes\">z<\/jats:italic>\n                        -scores in all the remaining regions (\n                        <jats:italic toggle=\"yes\">p<\/jats:italic>\n                        \u2009&lt;\u2009.001) and in the ipsilateral anterior cingulate (SUVR\n                        <jats:italic toggle=\"yes\">z<\/jats:italic>\n                        -score\u2009=\u2009.27, 95% CI\u2009=\u2009.04\u2013.49,\n                        <jats:italic toggle=\"yes\">p<\/jats:italic>\n                        \u2009=\u2009.020). No significant deposition was observed in other regions. Seven patients (23%) had low A\u03b21\u201342 levels, and two (7%) had elevated p181-tau levels in CSF. Higher p181-tau levels correlated with poorer verbal fluency (\n                        <jats:italic toggle=\"yes\">R<\/jats:italic>\n                        \u2009=\u2009\u2212.427,\n                        <jats:italic toggle=\"yes\">p<\/jats:italic>\n                        \u2009=\u2009.044). Significance: Our findings reveal a considerable A\u03b2 deposition in mesial temporal regions and ipsilateral anterior cingulate among adults with drug-resistant TLE. Additionally, abnormal CSF A\u03b21\u201342 levels were observed in a significant proportion of patients, and p181-tau levels were associated with verbal fluency. These results suggest that markers of neuronal damage can be observed in adults with TLE, warranting further investigation.\n                      <\/jats:p>\n                    <\/jats:boxed-text>\n                  <\/jats:p>","DOI":"10.1177\/15357597251333160","type":"journal-article","created":{"date-parts":[[2025,4,16]],"date-time":"2025-04-16T16:04:15Z","timestamp":1744819455000},"page":"266-268","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":2,"title":["Epilepsy and Amyloid: The Plot Thickens\u2026 So Will the Brain Thin?"],"prefix":"10.1177","volume":"25","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8291-7864","authenticated-orcid":false,"given":"Rani A.","family":"Sarkis","sequence":"first","affiliation":[{"name":"Epilepsy Division \rDepartment of Neurology \rBrigham and Women's Hospital \rHarvard Medical School"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2025,4,16]]},"reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1001\/jamaneurol.2019.1708"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1001\/jamaneurol.2023.0339"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1093\/brain\/awz381"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1111\/epi.17186"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1038\/s41582-021-00505-9"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1212\/WNL.0000000000210303"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1111\/epi.18142"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.1001\/jamaneurol.2016.6091"},{"key":"e_1_3_2_10_2","doi-asserted-by":"publisher","DOI":"10.1038\/s41593-020-0687-6"},{"key":"e_1_3_2_11_2","doi-asserted-by":"publisher","DOI":"10.1001\/jamaneurol.2018.0629"}],"container-title":["Epilepsy Currents"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/journals.sagepub.com\/doi\/pdf\/10.1177\/15357597251333160","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/journals.sagepub.com\/doi\/full-xml\/10.1177\/15357597251333160","content-type":"application\/xml","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/journals.sagepub.com\/doi\/pdf\/10.1177\/15357597251333160","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2026,4,28]],"date-time":"2026-04-28T20:32:35Z","timestamp":1777408355000},"score":1,"resource":{"primary":{"URL":"https:\/\/journals.sagepub.com\/doi\/10.1177\/15357597251333160"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2025,4,16]]},"references-count":10,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2025,8]]}},"alternative-id":["10.1177\/15357597251333160"],"URL":"https:\/\/doi.org\/10.1177\/15357597251333160","relation":{},"ISSN":["1535-7597","1535-7511"],"issn-type":[{"value":"1535-7597","type":"print"},{"value":"1535-7511","type":"electronic"}],"subject":[],"published":{"date-parts":[[2025,4,16]]}}}