Abstract | Previous post-mortem epilepsy series showed phosphorylated-tau (pTau) accumulation in relation to traumatic brain injury (TBI) rather than driven by seizure frequency. The Corsellis Epilepsy Collection, established in the mid-20th century, represents brain samples collected from patients living with a range of epilepsies from the 1880’s to 1990s. Our aim was to interrogate this historical archive to explore relationships between epilepsy, trauma and tau pathology. AT8 immunohistochemistry for pTau was carried out in 102 cases (55% male, with mean age at death of 62 years) on frontal, temporal, amygdala, hippocampal and lesional cortical regions and evaluated using current NINDS criteria for chronic traumatic encephalopathy (CTE) and Braak staging with beta-amyloid, AT8-GFAP and other pTau markers (CP13, PHF1, AT100, AT180) in selected cases. CTE pathology was identified in 15.7% and associated with astroglial tau, a younger age of onset of epilepsy, evidence of TBI and institutionalisation for epilepsy compared to cases without CTE, but not for seizure type or frequency; memory impairment was noted in 43% of CTE, a significantly younger age of death and more frequent sudden and unexpected death (p<0.05-0.001). In contrast, a higher Braak stage was associated with late onset epilepsy and cognitive decline. Other pTau patterns observed were not typical for Braak or CTE stages and may represent epilepsy- related activity driving pTau accumulation. Of note, 9% of cases showed no pTau, including cases with long epilepsy duration, poor seizure control and a history of prior TBI. In summary, this cohort includes patients with more severe forms of epilepsy and CTE prevalence was more frequent than reported in non-epilepsy community-based studies (0-8%) but lower than published series from contact sports participants (32-87%). Of note pTau pathology was negative in a proportion of epilepsy cases requiring further investigation of underlying neuroprotective factors in this group. |
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