HIPPOCAMPAL TAU RELATED SIGNAL INDEXES HYPEREXCITABILITY AND NREM SLEEP MEMORY DYSFUNCTION IN TEMPORAL LOBE EPILEPSY
W skrócie
[Preprint - wstępne wyniki] Badacze zbadali, czy gromadzenie się białka tau w mózgu (mierzone specjalnym skanem) wiąże się z częstością napadów padaczki, zaburzeniami snu i problemami z pamięcią u pacjentów z padaczką płata skroniowego. Wyniki pokazały, że wyższa ilość tau w hipokampie (obszarze mózgu ważnym dla pamięci) korelowała z częstszymi napadami, gorszą jakością snu i słabszymi wynikami testów pamięci. Badanie sugeruje, że tau w hipokampie może być markerem wskazującym na podatność obwodów mózgowych na zaburzenia pamięci związane ze snem u pacjentów z tą formą padaczki.
Oryginalny abstract (angielski)
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.
Metadane publikacji
Journal
Preprint (medRxiv/bioRxiv)
Data publikacji
13.09.2026
DOI
10.64898/2026.09.07.748279
Europe PMC ID
PPR1318318
Autorzy
Arafat T, Schiller K, Lam J, Von Ellenrieder N, Cai Z, DeKraker J, Fadaie F, Sziklas V, Crane J, Cruces RR