AI Insight
This study examined 25 temporal lobe epilepsy patients and found that higher tau protein accumulation in the hippocampus, measured using 18F-MK6240 PET imaging, was associated with increased seizure frequency, disrupted sleep patterns during non-REM sleep, and impaired memory performance. Specifically, elevated hippocampal tau uptake correlated with reduced sleep spindles, increased slow waves, and worse memory outcomes. The findings suggest hippocampal tau accumulation may serve as a biomarker linking seizure activity to sleep and memory dysfunction in temporal lobe epilepsy.
Why it matters
This research could lead to new ways of identifying epilepsy patients at risk for memory problems and may help explain why sleep disturbances are common in temporal lobe epilepsy. If validated, tau imaging could potentially guide treatment strategies targeting both seizure control and cognitive preservation in epilepsy patients.
Understand the Science
⚠️ Preprint – Noch nicht peer-reviewed
Dieser Artikel wurde noch nicht von unabhängigen Experten begutachtet. Die Ergebnisse sind vorläufig und sollten mit Vorsicht interpretiert werden.
Background Sleep and memory disturbances are common in temporal lobe epilepsy (TLE), yet their relationship with tau-targeted neuroimaging measures remains unclear. We investigated whether in-vivo temporal 18F-MK6240 tracer retention relates to seizure burden, non-rapid eye movement (NREM) sleep microstructure, and memory performance in TLE. Methods This cross-sectional study was conducted from 2019 to 2024 at the Montreal Neurological Institute-Hospital. Eligible patients had unilateral TLE diagnosed according to International League Against Epilepsy criteria and underwent overnight electroencephalography (EEG) recordings, research-protocol 3T magnetic resonance imaging, and 18F-MK6240 positron emission tomography. Regional 18F-MK6240 standardized uptake value ratios (SUVRs), using the cerebellum as the reference region, were quantified in the ipsilateral hippocampus (defined a priori as the primary region of interest), as well as in peri-hippocampal and lateral temporal regions. Electroclinical and neuropsychological measures, including seizure burden (high vs low), N2 interictal epileptiform discharge frequency (frequent vs non-frequent), and memory performance (impaired vs intact), were classified according to predefined clinical criteria. N2 spindle rate and N3 slow-wave rate were quantified from overnight EEG recordings. Findings Of 70 eligible patients, 25 were included (eight [32%] females; mean age 35.2 years [SD 12.1]). Higher ipsilateral hippocampal 18F-MK6240 uptake was observed in participants with greater focal seizure burden (median [IQR] 0.70 [0.67-0.78] vs 0.64 [0.58-0.65], rank-biserial correlation=-0.58, 95% CI -0.82 to -0.19; p=0.02), was associated with lower N2 spindle rate (r=-0.42, 95% CI -0.70 to -0.03; p=0.04) and higher N3 slow-wave rate (r=0.47; 95% CI 0.09 to 0.73; p=0.02), and was also higher in participants with impaired than intact memory performance (n=21; mean [SD] 0.80 [0.12] vs 0.68 [0.10], Cohen’s d=1.15, 95% CI 0.07 to 2.21; p=0.04). Associations outside the hippocampus were generally less consistent and less precise, with the largest non-hippocampal estimate observed in peri-hippocampal regions. Interpretation Higher hippocampal 18F-MK6240 uptake was associated with greater focal seizure burden, altered NREM sleep microstructure, and impaired memory performance in TLE. These findings suggest that hippocampal 18F-MK6240 uptake may represent a candidate marker of circuit vulnerability associated with NREM sleep-memory dysfunction in TLE, warranting validation in larger longitudinal studies.