Amyloid deposition in adults with drug‐resistant temporal lobe epilepsy

Abstract Objective Pathological amyloid‐β (Aβ) accumulation and hyperphosphorylated tau proteins have been described in resected temporal lobe specimens of epilepsy patients. We aimed to determine cerebrospinal fluid (CSF) Aβ1‐42 and p181‐tau levels and cerebral Aβ deposits on positron emission tomography (Aβ 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 25–55 years old. Each participant underwent 18 F‐flutemetamol PET, determination of CSF Aβ1‐42, p181‐tau, and total tau, and a comprehensive neuropsychological assessment. We evaluated normalized standard uptake value ratios (SUVRs) for different brain regions on Aβ PET. Results Thirty patients (mean age = 41.9 ± SD 8.1 years, 57% men) were included. The median disease duration was 9.5 (interquartile range = 4–24) years. Twenty‐six patients (87%) had a clinically significant cognitive impairment on neuropsychological evaluation, 18 (69%) of the amnesic type. On Aβ PET, high uptake was observed in both mesial temporal regions (ipsilateral: SUVR z ‐score = .90, 95% confidence interval [CI] = .60–1.20; contralateral: SUVR z ‐score = .92, 95% CI = .57–1.27; p < .001), which was higher when compared to SUVR z ‐scores in all the remaining regions ( p < .001) and in the ipsilateral anterior cingulate (SUVR z ‐score = .27, 95% CI = .04–.49, p = .020). No significant deposition was observed in other regions. Seven patients (23%) had low Aβ1‐42 levels, and two (7%) had elevated p181‐tau levels in CSF. Higher p181‐tau levels correlated with poorer verbal fluency ( R = −.427, p = .044). Significance Our findings reveal a considerable Aβ deposition in mesial temporal regions and ipsilateral anterior cingulate among adults with drug‐resistant TLE. Additionally, abnormal CSF Aβ1‐42 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.