Neurogenesis in the human hippocampus and its relevance to temporal lobe epilepsies

Siebzehnrubl, Florian A.; Blümcke, Ingmar

doi:10.1111/j.1528-1167.2008.01638.x

Cited by 66 publications

(43 citation statements)

References 103 publications

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“…Recent data indicate that acute seizures or precipitating insults can induce neurogenesis, whereas the capacity of neuronal recruitment and proliferation substantially decreases in chronic phases of epilepsy [40].…”

Section: Wnt/b-catenin Signaling Pathway Involved In Neurogenesis Of mentioning

confidence: 99%

The Role of Wnt/β-Catenin Signaling Pathway in Disrupted Hippocampal Neurogenesis of Temporal Lobe Epilepsy: A Potential Therapeutic Target?

Huang

Zhou

et al. 2015

Neurochem Res

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Temporal lobe epilepsy is one of the most common clinical neurological disorders. One of the major pathological findings in temporal lobe epilepsy is hippocampal sclerosis, characterized by massive neuronal loss and severe gliosis. The epileptogenesis process of temporal lobe epilepsy usually starts with initial precipitating insults, followed by neurodegeneration, abnormal hippocampus circuitry reorganization, and the formation of hypersynchronicity. Experimental and clinical evidence strongly suggests that dysfunctional neurogenesis is involved in the epileptogenesis. Recent data demonstrate that neurogenesis is induced by acute seizures or precipitating insults, whereas the capacity of neuronal recruitment and proliferation substantially decreases in the chronic phase of epilepsy. Participation of the Wnt/β-catenin signaling pathway in neurogenesis reveals its importance in epileptogenesis; its dysfunction contributes to the structural and functional abnormality of temporal lobe epilepsy, while rescuing this pathway exerts neuroprotective effects. Here, we summarize data supporting the involvement of Wnt/β-catenin signaling in the epileptogenesis of temporal lobe epilepsy. We also propose that the Wnt/β-catenin signaling pathway may serve as a promising therapeutic target for temporal lobe epilepsy treatment.

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Section: Wnt/b-catenin Signaling Pathway Involved In Neurogenesis Of mentioning

confidence: 99%

The Role of Wnt/β-Catenin Signaling Pathway in Disrupted Hippocampal Neurogenesis of Temporal Lobe Epilepsy: A Potential Therapeutic Target?

Huang

Zhou

et al. 2015

Neurochem Res

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“…Some nestin positive cells differentiated into astrocytes, while some differentiated into neurons and participated in neurogenesis and gliosis. Both neurogenesis and gliosis played important roles in the pathogenesis of epilepsy [12,13,23]. Activated gliocytes can produce and release neurotransmitters, cytokines, neurotrophic factors, toxic metabolites.…”

Section: Discussionmentioning

confidence: 99%

Nestin in the Temporal Neocortex of the Intractable Epilepsy Patients

Wang

Yuan

et al. 2008

Neurochem Res

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Nestin is one kind of intermediate filament protein, which is considered as a typical marker of neural precursor cells. Considerable evidence supports nestin may have actively functions in neurogenesis and gliosis. Our aim was to investigate nestin expression in the temporal neocortex of patients with intractable epilepsy (IE), and then to discuss the possible role of nestin in IE. Tissue samples from the temporal neocortex of 32 patients who had surgery for IE were used to detect nestin expression by immunohistochemistry, immunofluorescence. We compared these tissues with 12 histologically normal temporal neocortex from intracranial hypertension patients who had decompression procedures. In this study, we found some nestin positive cells in the normal temporal neocortex, but in the intractable epilepsy, they were upregulated, increasing with length of course and seizure frequency. Optical density (OD) value in epileptic tissue was determined 0.246 +/- 0.030, and 0.134 +/- 0.040 in the control (P < 0.05). Double lables of immunofluorescence showed some nestin positive cells coexpression with glial fibrillary acidic protein (GFAP), while some coexpression with microtubule-associated protein-2 (MAP(2)). These findings provided some evidence for increased neurogenesis and gliosis in epilepsy, which could be associated with intractable epilepsy.

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“…Probably the involvement of GH signalling not regards the GH-receptor (GHR); in fact, an increase of neuronal proliferation in the subgranular zone of the dentate gyrus has been shown in GHR knockout mice (Ransome & Turnley, 2008). The neuronal plasticity related to GH suggests the possibility of therapeutic interventions against neurodegenerative disorders in the older age; however, recent data also indicate that these newly generated neurons are integrated into epileptogenic networks in animal models (Siebzehnrubl & Blumcke, 2008), suggesting that neurogenesis contributes to promote susceptibility to seizures.…”

Section: Growth Hormone and Insulin-like Growth Factor-1mentioning

confidence: 99%