Granule cell dispersion is not accompanied by enhanced neurogenesis in temporal lobe epilepsy patients

Fahrner, Alexander; Kann, Gunda; Flubacher, Armin; Heinrich, Christophe; Freiman, Thomas M.; Zentner, Josef; Frotscher, Michael; Haas, Carola A.

doi:10.1016/j.expneurol.2006.08.023

Cited by 112 publications

(108 citation statements)

References 39 publications

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“…Recent work examining hippocampal C 14 accumulation from Cold War-era nuclear tests has established that neurogenesis continues throughout life in humans (7). Studies examining tissue resected from temporal lobe epilepsy patients also paint a relatively consistent picture showing impaired neurogenesis in chronic epilepsy (8), although it is much more difficult to assay for persistent neurogenesis in human tissue specimens than in animal models. Robust studies to determine whether neurogenesis is increased in newly diagnosed epilepsy will need to await the development of noninvasive approaches to measure cell proliferation, because tissue (fortunately) is typically not available.…”

Section: Neurogenesis In Epilepsy: Better To Burn Out or Fade Away?mentioning

confidence: 99%

Neurogenesis in Epilepsy: Better to Burn Out or Fade Away?

Danzer¹

2016

Epilepsy Curr

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Section: Neurogenesis In Epilepsy: Better To Burn Out or Fade Away?mentioning

confidence: 99%

Neurogenesis in Epilepsy: Better to Burn Out or Fade Away?

Danzer¹

2016

Epilepsy Curr

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“…Doublecortin is a microtubule-associated protein expressed by immature migrating neurons. 12,23,41,43,76 All washes and antibody incubations were conducted in Trisbuffered saline (TBS: 0.15 M NaCl, 0.1 M Tris-HCl, pH 7.5). Briefly, mounted tissue was warmed for 10 minutes at 60°C before being cleared in xylene (Fisher Scientific) and rehydrated through an alcohol gradient.…”

Section: Immunohistochemical Analysismentioning

confidence: 99%

Maturation-dependent response of neurogenesis after traumatic brain injury in children

Taylor

Smith²,

Harris

et al. 2013

PED

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Object Traumatic brain injury (TBI) is the leading cause of acquired disability in children, yet innate repair mechanisms are incompletely understood. Given data from animal studies documenting neurogenesis in response to trauma and other insults, the authors investigated whether similar responses could be found in children of different ages after TBI. Methods Immunohistochemistry was used to label doublecortin (DCX), a protein expressed by immature migrating neuroblasts (newborn neurons), in specimens from patients ranging in age from 3 weeks to 10 years who had died either after TBI or from other causes. Doublecortin-positive (DCX+) cells were examined in the subventricular zone (SVZ) and periventricular white matter (PWM) and were quantified within the granule cell layer (GCL) and subgranular zone (SGZ) of the dentate gyrus to determine if age and/or injury affect the number of DCX+ cells in these regions. Results The DCX+ cells decreased in the SVZ as patient age increased and were found in abundance around a focal subacute infarct in a 1-month-old non-TBI patient, but were scarce in all other patients regardless of age or history of trauma. The DCX+ cells in the PWM and dentate gyrus demonstrated a migratory morphology and did not co-localize with markers for astrocytes, microglia, or macrophages. In addition, there were significantly more DCX+ cells in the GCL and SGZ of the dentate gyrus in children younger than 1 year old than in older children. The density of immature migrating neuroblasts in infants (under 1 year of age) was significantly greater than in young children (2–6 years of age, p = 0.006) and older children (7–10 years of age, p = 0.007). Conclusions The main variable influencing the number of migrating neuroblasts observed in the SVZ, PWM, and hippocampus was patient age. Trauma had no discernible effect on the number of migrating neuroblasts in this cohort of patients in whom death typically occurred within hours to days after TBI.

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“…Alternatively, neurogenesis in the lesioned hippocampus has been reported as selectively absent in zones of granule cell dispersion, suggesting a disruption of the subgranular zone neurogenic niche. 19,32 Indeed, there is indirect evidence from research in human Ammon horn sclerosis indicating that granule cell dispersion results from an abnormal migration of mature granule cells along an elongated radial glial scaffold, rather than from malpositioning of newly born granule cells. 19 Similarly, data from mouse kainate studies suggest that displacement of mature granule cells results from a local deficiency in reelin, an extracellular matrix protein important for neuronal migration.…”

Section: Hippocampal Neurogenesis and Epilepsymentioning

confidence: 99%

“…19,32 Indeed, there is indirect evidence from research in human Ammon horn sclerosis indicating that granule cell dispersion results from an abnormal migration of mature granule cells along an elongated radial glial scaffold, rather than from malpositioning of newly born granule cells. 19 Similarly, data from mouse kainate studies suggest that displacement of mature granule cells results from a local deficiency in reelin, an extracellular matrix protein important for neuronal migration. 24 Two recent studies in different rodent models highlight the importance of the local network environment in determining the functional status of newborn neurons that develop following seizure.…”

Section: Hippocampal Neurogenesis and Epilepsymentioning

confidence: 99%

Developing cell transplantation for temporal lobe epilepsy

Richardson¹,

Barbaro²,

Alvarez-Buylla³

et al. 2008

FOC

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✓ Mesial temporal lobe epilepsy (MTLE) is presumed to develop progressively as a consequence of synaptic reorganization and neuronal loss, although the exact etiology of seizure development is unknown. Nearly 30% of patients with MTLE have disabling seizures despite pharmacological treatment, and the majority of these patients are recommended for resection. The authors review cell transplantation as an alternative approach to the treatment of epilepsy. Recent work in animal models shows that grafted neuronal precursors that differentiate into inhibitory interneurons can increase the level of local inhibition. Grafts of these inhibitory neurons could help restore equilibrium in MTLE. Developing a sound transplantation strategy involves careful consideration of the etiology of MTLE and the expected functional role of transplanted cells. These issues are reviewed, with a focus on those factors most likely to influence clinically applicable results.

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Granule cell dispersion is not accompanied by enhanced neurogenesis in temporal lobe epilepsy patients

Cited by 112 publications

References 39 publications

Neurogenesis in Epilepsy: Better to Burn Out or Fade Away?

Neurogenesis in Epilepsy: Better to Burn Out or Fade Away?

Maturation-dependent response of neurogenesis after traumatic brain injury in children

Developing cell transplantation for temporal lobe epilepsy

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