Elevation of tau protein levels in the cerebrospinal fluid of children with West syndrome

Inoue, Hirofumi; Matsushige, Takeshi; Hasegawa, Shunji; Abe, Arisa; Iida, Yasunori; Inoue, T; Ichiyama, Takashi

doi:10.1016/j.eplepsyres.2012.07.002

Cited by 6 publications

(6 citation statements)

References 18 publications

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“…Several studies suggest the occurrence of cell injury, including apoptosis, in MCD associated with epilepsy [32–35]. Recently we provided evidence of neurodegenerative changes in MCD associated with mTOR pathway hyperactivation (FCD type II and TSC), supporting a link between neurodevelopmental and neurodegenerative pathways [22].…”

Section: Discussionmentioning

confidence: 61%

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: 61%

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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“…Several studies provide evidence of cell injury, including apoptosis, in MCD associated with epilepsy (12,19,27,39). However evaluation in specific FCD subtypes (FCD I and II) compared with TSC, as well as the possible correlation with seizure history is still lacking.…”

Section: Discussionmentioning

confidence: 98%

“…Interestingly, both CDK5 and the mTOR signaling pathways are known to be activated in focal malformations of cortical development (MCD), such as focal cortical dysplasia (FCD) and cortical tubers in the tuberous sclerosis complex [TSC; (28,45,55); for a review, see (9,20)]. Moreover, several studies suggest that cell injury, including apoptosis, may occur in MCD associated with epilepsy (12,19,27,39). In particular, evidence of pathologically phosphorylated tau has been reported in older FCD patients (53).…”

Section: Introductionmentioning

confidence: 98%

Cell injury and Premature Neurodegeneration in Focal Malformations of Cortical Development

et al. 2013

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Several lines of evidence suggest that cell injury may occur in malformations of cortical development associated with epilepsy. Moreover, recent studies support the link between neurodevelopmental and neurodegenerative mechanisms. We evaluated a series of focal cortical dysplasia (FCD, n=26; type I and II) and tuberous sclerosis complex (TSC, n=6) cases. Sections were processed for terminal deoxynucleotidyl transferase-mediated 2'-deoxyuridine 5'-triphosphate nick-end labeling (TUNEL) labeling and immunohistochemistry using markers for the evaluation of apoptosis signaling pathways and neurodegeneration-related proteins/pathways. In both FCD II and TSC specimens, we observed significant increases in both TUNEL-positive and caspase-3-positive cells compared with controls and FCD I. Expression of β-amyloid precursor protein was observed in neuronal soma and processes in FCD II and TSC. In these specimens, we also observed an abnormal expression of death receptor-6. Immunoreactivity for phosphorylated tau was only found in older patients with FCD II and TSC. In these cases, prominent nuclear/cytoplasmic p62 immunoreactivity was detected in both dysmorphic neurons and balloon/giant cells. Our data provide evidence of complex, but similar, mechanisms of cell injury in focal malformations of cortical development associated with mammalian target of rapamycin pathway hyperactivation, with prominent induction of apoptosis-signaling pathways and premature activation of mechanisms of neurodegeneration.

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“…West syndrome (WS) is an epileptic syndrome of early childhood with poor prognosis and characterized by the triad of infantile spasms, hypsarrhythmia, and an arrest of psychomotor development [1,2]. The incidence of infantile spasms ranges from 2 to 3.5 per 10,000 live births, with onset during the first year of life in 90% of those affected.…”

Section: Introductionmentioning

confidence: 99%

Serum and cerebrospinal fluid excitatory amino acid, nitric oxide and cerebrospinal fluid malondialdehyde levels in West syndrome

et al. 2015

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West syndrome (WS) is an epileptic syndrome of early childhood. There have been a limited numbers of studies of cerebrospinal fluid (CSF) excitatory amino acid (EAA), nitric oxide (NO), and malondialdehyde (MDA) levels, as well as plasma levels of EAA, and NO, in WS. In this article, CSF EAA, NO, and MDA levels and plasma EAA, NO status, and a determination of the effects of antiepileptic drug therapy on these values were investigated in children with WS. Evaluation of CSF and serum EAA, NO, and MDA levels and of serum EAA and NO levels after 3 mo of antiepileptic drug therapy revealed a statistically significant decrease in CSF aspartate, glutamate, NO and MDA levels. In conclusion, the decrease in CSF MDA levels in this study is the result of both the decrease in glutamate activity and neuronal damage after controlling seizures with antiepileptic drugs.

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Elevation of tau protein levels in the cerebrospinal fluid of children with West syndrome

Cited by 6 publications

References 18 publications

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

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

Cell injury and Premature Neurodegeneration in Focal Malformations of Cortical Development

Serum and cerebrospinal fluid excitatory amino acid, nitric oxide and cerebrospinal fluid malondialdehyde levels in West syndrome

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