{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T10:26:24Z","timestamp":1791195984439,"version":"4.1.0"},"reference-count":36,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2021,9,30]],"date-time":"2021-09-30T00:00:00Z","timestamp":1632960000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001782","name":"University of Melbourne","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100001782","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100015539","name":"Australian Government","doi-asserted-by":"publisher","award":["MRF1136427"],"award-info":[{"award-number":["MRF1136427"]}],"id":[{"id":"10.13039\/100015539","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Epilepsia"],"published-print":{"date-parts":[[2021,12]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Objective<\/jats:title><jats:p>Cognitive impairment is common in patients with chronic drug\u2010resistant temporal lobe epilepsy (TLE). Hyperphosphorylated tau (pTau) and amyloid\u2010\u03b2 (A\u03b2) plaques, pathological hallmarks of Alzheimer disease, have been hypothesized to play a mechanistic role. We investigated A\u03b2 plaques and pTau prevalence in TLE patients who underwent resective surgery and correlated their presence with preoperative psychometric test scores and clinical factors.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Patients were retrospectively selected from the epilepsy surgery register of the Royal Melbourne Hospital, Australia. Sections from the resected temporal lobe were immunostained for pTau and A\u03b2 plaques (antibodies: AT8, 1E8). The presence and severity of pathology were correlated with clinical characteristics, and verbal and visual learning functions as measured by the Verbal Pair Associates (VPA) test and Rey Complex Figure Test.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Fifty\u2010six patients (55% female) aged 20\u201368\u00a0years (median = 34\u00a0years) at surgery were included. A\u03b2 plaques were detected in four patients (7%), all at the moderate level. There was no difference in duration, age at onset of epilepsy, or side of resection between patients with and without A\u03b2 plaques. Sparse pTau was found in two patients (3.5%). Both had moderate A\u03b2 plaques and were &gt;50\u00a0years of age. Patients with A\u03b2 plaques had a lower median score for the VPA hard assessment compared to those without (0 vs. 4; <jats:italic>p<\/jats:italic>\u00a0=\u00a0.02). There was otherwise no correlation between pathology and psychometric test scores.<\/jats:p><\/jats:sec><jats:sec><jats:title>Significance<\/jats:title><jats:p>A\u03b2 plaques and pTau were uncommon in the resected brain tissue of patients who have undergone temporal lobectomy, and did not correlate with clinical characteristics or preoperative psychometric test scores, except for a lower VPA median score in patients with A\u03b2 plaques. Therefore, considering the low prevalence of A\u03b2 plaques and pTau herein observed, it is unlikely that cognitive impairment in TLE is driven by the same mechanisms as in Alzheimer disease.<\/jats:p><\/jats:sec>","DOI":"10.1111\/epi.17086","type":"journal-article","created":{"date-parts":[[2021,10,1]],"date-time":"2021-10-01T09:06:30Z","timestamp":1633079190000},"page":"3058-3067","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":29,"title":["Low prevalence of amyloid and tau pathology in drug\u2010resistant temporal lobe epilepsy"],"prefix":"10.1111","volume":"62","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2146-4221","authenticated-orcid":false,"given":"Juliana C.","family":"Silva","sequence":"first","affiliation":[{"name":"Department of Neuroscience Central Clinical School Monash University Melbourne Victoria Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1182-0907","authenticated-orcid":false,"given":"Lucy","family":"Vivash","sequence":"additional","affiliation":[{"name":"Department of Neuroscience Central Clinical School Monash University Melbourne Victoria Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0534-3718","authenticated-orcid":false,"given":"Charles B.","family":"Malpas","sequence":"additional","affiliation":[{"name":"Department of Neuroscience Central Clinical School Monash University Melbourne Victoria Australia"},{"name":"Department of Medicine Royal Melbourne Hospital University of Melbourne Melbourne Victoria Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yong","family":"Hao","sequence":"additional","affiliation":[{"name":"Department of Neurology Renji Hospital Medical School Shanghai Jiaotong University Shanghai China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Catriona","family":"McLean","sequence":"additional","affiliation":[{"name":"Department of Anatomical Pathology Alfred Health Melbourne Victoria Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhibin","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Neuroscience Central Clinical School Monash University Melbourne Victoria Australia"},{"name":"School of Public Health &amp; Preventive Medicine Monash University Melbourne Victoria Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Terence J.","family":"O'Brien","sequence":"additional","affiliation":[{"name":"Department of Neuroscience Central Clinical School Monash University Melbourne Victoria Australia"},{"name":"Department of Medicine Royal Melbourne Hospital University of Melbourne Melbourne Victoria 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