An immunohistochemical finding in glioneuronal lesions associated with epilepsy: The appearance of nestin‐positive, CD34‐positive and tau‐accumulating cells

Abstract

Several kinds of unusual cells have been pathologically identified in epileptic patients. CD34-positive, nestin-positive and tau-positive cells are some of them. However, no reports have investigated the significance of these cells. We examined 14 cases of seizure-associated glioneuronal lesions to investigate the incidences and distributions of these cells and the association between their incidence and clinical parameters. CD34-positive and nestin-positive cells were seen in 43% and 50% of cases, respectively. In the regions with structural anomalies, there were increased numbers of CD34-positive cells and nestin-positive cells, but they were identified as different cells. Both examinations showed many abnormal processes in oligodendroglial-like cells with round nuclei. In contrast, few reactive astrocytes that demonstrated immunoreactivity for glial fibrillary acidic protein were found in this area. Tau accumulation was present in 37% of cases. There was no correspondence with the regions showing increasing numbers of nestin or CD34-positive cells. There were no significant associations between epileptic clinical parameters and the incidences of the abovementioned immunopositive cells. CD34-positive cells and nestin-positive cells are found as frequently as balloon cells and are associated with abnormal reconstitution of the cortex. These findings support the assertion that increases in the numbers of these cells might contribute to promoting epilepsy. In addition, these immunopositive cells are valuable findings for the pathological identification of epileptogenic lesions.

Diffuse form of dysembryoplastic neuroepithelial tumour: the histological and immunohistochemical features of a distinct entity showing transition to dysembryoplastic neuroepithelial tumour and ganglioglioma

“…The dissimilar cytomorphology of the nestin‐ and CD34‐expressing cells was also described by Nagaishi et al . in classical DNT and FCD [17]. This indicates that CD34 and nestin probably label different cell populations, although double expression in certain cells may occur.…”

Analyzing dendritic spine pathology in Alzheimer’s disease: problems and opportunities

“…The deposition of hyperphosphorylated tau protein in neurons may be secondary to several different types of insults, such as epilepsy [134, 227], chronic traumatic brain injury [71], focal cortical dysplasia [174] or Niemann–Pick disease type C [117, 187]. Tau protein itself seems to be a prerequisite for neuronal damage, as tau knockout mice are immune to neuronal insults mediated by NMDA receptor-dependent excitotoxicity, as well as those caused by amyloid beta [110, 159, 160].…”

Potential Similarities in Temporal Lobe Epilepsy and Alzheimer’s Disease

“…Nagaishi et al has examined 14 clinical cases of seizureassociated glioneuronal lesions, and they found taccumulation in 37% of cases. 48 Triple transgenic model of AD mice with pilocarpine-induced chronic epilepsy had more neuritic plaque formation and altered intraneuronal p-t expression in temporal lobe structures, with elevated b-secretase 1 and Ab immunoreactivity. 49 …”