Back to Search
Start Over
The role of neurogenesis in neurorepair after ischemic stroke
- Source :
- Seminars in Cell & Developmental Biology. 95:98-110
- Publication Year :
- 2019
- Publisher :
- Elsevier BV, 2019.
-
Abstract
- Stroke consists of an abrupt reduction of cerebral blood flow resulting in hypoxia that triggers an excitotoxicity, oxidative stress, and neuroinflammation. After the ischemic process, neural precursor cells present in the subventricular zone of the lateral ventricle and subgranular zone of the dentate gyrus proliferate and migrate towards the lesion, contributing to the brain repair. The neurogenesis is induced by signal transduction pathways, growth factors, attractive factors for neuroblasts, transcription factors, pro and anti-inflammatory mediators and specific neurotransmissions. However, this endogenous neurogenesis occurs slowly and does not allow a complete restoration of brain function. Despite that, understanding the mechanisms of neurogenesis could improve the therapeutic strategies for brain repair. This review presents the current knowledge about brain repair process after stroke and the perspectives regarding the development of promising therapies that aim to improve neurogenesis and its potential to form new neural networks.
- Subjects :
- 0301 basic medicine
Neurogenesis
Excitotoxicity
Subventricular zone
Biology
medicine.disease_cause
Brain Ischemia
Subgranular zone
Brain ischemia
03 medical and health sciences
0302 clinical medicine
Neuroblast
medicine
Animals
Humans
Neuroinflammation
Dentate gyrus
Cell Biology
medicine.disease
Nerve Regeneration
Stroke
030104 developmental biology
medicine.anatomical_structure
Cell Transdifferentiation
Neuroscience
030217 neurology & neurosurgery
Stem Cell Transplantation
Developmental Biology
Subjects
Details
- ISSN :
- 10849521
- Volume :
- 95
- Database :
- OpenAIRE
- Journal :
- Seminars in Cell & Developmental Biology
- Accession number :
- edsair.doi.dedup.....984b0f3f6da65627788295d326bf1f50
- Full Text :
- https://doi.org/10.1016/j.semcdb.2018.12.003