In light of the current interest in the bidirectional relationship between epilepsy and dementia, primary attention is currently focused on the role of hyperphosphorylated tau (pTau) in cognition in epilepsy. Synthesizing available data from studies investigating pTau burden in surgical biopsy specimens from patients with temporal lobe epilepsy, the prevalence of pTau across five studies with a total number of 142 patients ranges from 3.5% to 95%. Findings also varied with regard to the location of pTau in the hippocampus and/or temporal cortex. Two of five studies (40%) demonstrated an inverse relationship between pTau burden and cognitive performance, one study with regard to executive functions and the other with regard to naming and verbal short-term memory. This is partly unexpected since executive functions and verbal short-term memory depend less on temporal than extratemporal fronto-parietal networks. The only longitudinal study found a significant link between pTau and cognitive decline in verbal learning and memory and in part also in naming from pre- to postoperative and from three to 12 months postoperative. Given the heterogeneity of the study cohorts, the neuropsychological and neuropathological methods and findings, no clear picture emerges regarding the association between pTau and cognition in temporal lobe epilepsy. This could in part be expected due to the multifactorial etiology of cognitive impairment in epilepsy, including the active epilepsy, the underlying and sometimes dynamic pathology, and anti-seizure medication. Some of these factors may affect pTau expression. Further research should investigate pTau longitudinally and noninvasively on a whole-brain level, using standardized, targeted neuropsychological outcome measures, while controlling for age and other factors that may influence cognitive trajectories in epilepsy.