Is intractable epilepsy a tauopathy?

Xi, Zhiqin; Wang, Xuefeng; Shu, Xiao-Fang; Chen, Guojun; Xiao, Fei; Sun, Jijun; Zhu, Xiongwei

doi:10.1016/j.mehy.2011.03.003

Cited by 19 publications

(12 citation statements)

References 63 publications

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“…Whether a deregulation of tau degradation may reflect an early defect in microtubules (as suggested in HME [60]), and may contribute to epileptogenesis in GNT requires further investigation. Accordingly, epileptiform discharges and spontaneous recurrent seizures have been reported in a mouse models of AD [65] and it has been known for some time that seizures occur in some patients with tauopathies [66], supporting the role of dysfunctional tau in intractable epilepsy [67]. Moreover, as a high level of phosphorylation of the tau protein is observed during foetal development [68,69], an abnormal phosphorylation of tau may reflect the immature properties of the neuronal component of the tumour or even a recapitulation of a developmental programme contributing to pathological neuroplasticity [69–71].…”

Section: Discussionmentioning

confidence: 93%

See 1 more Smart Citation

Expression of neurodegenerative disease‐related proteins and caspase‐3 in glioneuronal tumours

Prabowo

Iyer

Veersema

et al. 2015

Neuropathology Appl Neurobio

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Section: Discussionmentioning

confidence: 93%

“…Several hypotheses have been put forward during the past decades to explain epileptogenesis in GNT, suggesting the involvement of multiple mechanisms [3]. Whether a deregulation of neurodegeneration‐related proteins/pathways could also contribute to epileptogenesis in GNT requires further investigation [67].…”

Section: Discussionmentioning

confidence: 99%

Expression of neurodegenerative disease‐related proteins and caspase‐3 in glioneuronal tumours

Prabowo

Iyer

Veersema

et al. 2015

Neuropathology Appl Neurobio

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“…15 The presence of neocortical tau deposition in the present study was significantly increased compared to the autopsy study (P < .0001). 17 In a previous pilot study of young patients who had undergone epilepsy surgery, 1 patient (10%) demonstrated tau pathology consistent with CTE. 16 Pretangle tau pathology was limited to the brainstem and medial temporal lobe structures in individuals younger than 30 years; a very low percentage of individuals between 31 and 40 years of age showed tau advancement into the neocortex.…”

Section: T a B L E 1 Relevant Studies On Tau Pathology In Patients Wimentioning

confidence: 94%

Tau deposition in young adults with drug‐resistant focal epilepsy

et al. 2019

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This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. Abstract Objective: To evaluate the presence of tau deposition and pathologic features of chronic traumatic encephalopathy (CTE) in young adult patients treated with focal cortical resections for drug-resistant epilepsy. Methods: Sixty consecutive patients who had undergone surgical treatment for drugresistant focal epilepsy between 18 and 45 years of age were identified (2010-2017).Medical records were reviewed to determine clinical factors, including history of head trauma, age at seizure onset, age at surgical resection, seizure type(s) and frequency, imaging findings, and surgical outcome. All formalin-fixed, paraffin-embedded blocks from the surgical specimens from each subject were sectioned and stained with hematoxylin and eosin and antibodies to tau (Thermo Fisher Scientific Clone AT8), and examined blindly for tau pathology, including lesions characteristic of CTE. Results: The median age at resection was 29.5 years (range = 19-45). A history of head trauma was reported in 19 patients. Although none of the patients had pathological findings characteristic of CTE, 23 patients (38%) demonstrated tau-immunoreactive lesions, including neurites, neurofibrillary pretangles, neurofibrillary tangles, subpial tau, and/or glial tau. In 4 of the 23 patients (7% of the cohort; 17% of those with tau pathology), substantial tau burden was identified. Three of these 4 patients had no significant history of head trauma; 1 patient had multiple sports-related concussions. No specific clinical factors correlated with the presence of tau pathology. Significance: Tau-immunoreactive lesions were found in 38% of 60 patients who underwent a focal cortical resection for drug-resistant focal epilepsy. Diagnostic features of CTE were not detected in any patient; however, the pathological evaluation for CTE was limited to a surgical specimen. The prominent and excessive tau deposition in 23 patients (38%) is abnormal in this age group and warrants further investigation. K E Y W O R D Schronic traumatic encephalopathy, epilepsy surgery, neuropathology | 2399 SMITH eT al.

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“…However, the neocortical layer of most severe neuronal loss and in adult tauopathies is layer 2 [34] and the phosphorylated tau expression in all of our infantile cases of HME was also in the superficial laminae of the cortex, showing a similar gradient within the cortex. Tau over-expression is not specific to HME in paediatric brain tissue, but the only other malformations which share this feature, to our knowledge, are tuberous sclerosis and focal cortical dysplasia type IIb, with balloon cells and dysplastic neurons, which also share the same property of mTOR activation [40,49]. Tau over-expression is also reported many years following traumatic contusions of the brain [22].…”

Section: Discussionmentioning

confidence: 77%