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Updated: Mar 8, 2026
Generation of Neural Stem Cells from Discarded Human Fetal Cortical Tissue
Published on: May 25, 2011
Neural Stem Cells and Fetal-Onset Hydrocephalus
Esteban M Rodríguez1, María M Guerra
1Instituto de Anatomía, Histología y Patología, Facultad de Medicina, Universidad Austral de Chile, Valdivia, Chile.
Insights
Fetal-onset hydrocephalus involves brain and cerebrospinal fluid disorders. A novel hypothesis suggests neural stem cell (NSC) junction pathology causes both hydrocephalus and impaired neurogenesis in affected infants.
Area of Science:
- Neuroscience
- Developmental Biology
- Cell Biology
Background:
- Fetal-onset hydrocephalus is a complex brain disorder affecting cerebrospinal fluid (CSF) dynamics.
- The underlying causes of inborn, irreparable neurological impairment in hydrocephalus remain incompletely understood.
- Neural stem cells (NSCs) and neural progenitor cells (NPCs) are the origin of all central nervous system cells.
Purpose of the Study:
- To investigate the hypothesis that cell junction pathology in NSCs is a root cause of fetal-onset hydrocephalus.
- To explore the link between NSC dysfunction, ventricular zone (VZ) disruption, and abnormal neurogenesis.
- To identify potential therapeutic targets for hydrocephalus by studying disrupted NSC and NPC behavior.
Main Methods:
- The study proposes investigating the role of cell junction pathology in neural stem cells (NSCs).
- Analysis of ventricular zone (VZ) disruption patterns and their correlation with hydrocephalus and neurogenesis.
- Examination of released NSCs and NPCs in CSF, including their potential transformation into neurospheres.
Main Results:
- A hypothesized common pathway involves genetic mutations or foreign signals leading to NSC cell junction pathology and VZ disruption.
- VZ disruption exhibits specific temporal and spatial patterns, causing aqueduct obliteration and hydrocephalus.
- Abnormal neurogenesis in the telencephalon is linked to VZ disruption.
Conclusions:
- Cell junction pathology in NSCs and subsequent VZ disruption are proposed as the unifying mechanism for hydrocephalus and abnormal neurogenesis.
- Disrupted NSCs and NPCs released into CSF may offer insights into molecular disease mechanisms.
- These cells present a potential avenue for developing novel NSC-based therapies for hydrocephalus.
Abstract:
Fetal-onset hydrocephalus is not only a disorder of cerebrospinal fluid (CSF) dynamics, but also a brain disorder. How can we explain the inborn and, so far, irreparable neurological impairment in children born with hydrocephalus? We hypothesize that a cell junction pathology of neural stem cells (NSC) leads to two inseparable phenomena: hydrocephalus and abnormal neurogenesis. All neurons, glial cells, and ependymal cells of the mammalian central nervous system originate from the NSC forming the ventricular zone (VZ) and the neural progenitor cells (NPC) forming the subventricular zone. Several genetic mutations and certain foreign signals all convey into a final common pathway leading to cell junction pathology of NSC and VZ disruption. VZ disruption follows a temporal and spatial pattern; it leads to aqueduct obliteration and hydrocephalus in the cerebral aqueduct, while it results in abnormal neurogenesis in the telencephalon. The disrupted NSC and NPC are released into the CSF and may transform into neurospheres displaying a junctional pathology similar to that of NSC of the disrupted VZ. These cells can then be utilized to investigate molecular alterations underlying the disease and open an avenue into possible NSC therapy.
