scholarly journals Is Forebrain Neurogenesis a Potential Repair Mechanism after Stroke?

2015 ◽  
Vol 35 (7) ◽  
pp. 1220-1221 ◽  
Author(s):  
agos Inta ◽  
Peter Gass
Keyword(s):  
Adult Neurogenesis ◽  
Broad Spectrum ◽  
Subventricular Zone ◽  
Genetic Manipulation ◽  
Gabaergic Interneurons ◽  
Repair Mechanism ◽  
Brain Repair ◽  
Human Neocortex ◽  
Repair Strategy ◽  
Adult Human

The use of adult subventricular zone (SVZ) neurogenesis as brain repair strategy after stroke represents a hot topic in neurologic research. Recent radiocarbon-14 dating has revealed a lack of poststroke neurogenesis in the adult human neocortex; however, adult neurogenesis has been shown to occur, even under physiologic conditions, in the human striatum. Here, these results are contrasted with experimental poststroke neurogenesis in the murine brain. Both in humans and in rodents, the SVZ generates predominantly calretinin (CR)-expressing GABAergic interneurons, which cannot replace the broad spectrum of neuronal subtypes damaged by stroke. Therefore, SVZ neurogenesis may represent a repair mechanism only after genetic manipulation redirecting its differentiation.

scholarly journals Targeting Adult Neurogenesis for Poststroke Therapy

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Jianfei Lu ◽  
Anatol Manaenko ◽  
Qin Hu
Keyword(s):  
Stem Cells ◽  
Adult Neurogenesis ◽  
Subventricular Zone ◽  
Tissue Repair ◽  
Therapeutic Interventions ◽  
Subgranular Zone ◽  
Brain Repair ◽  
Function Recovery ◽  
Newborn Neurons ◽  
And Function

Adult neurogenesis mainly occurs at the subventricular zone (SVZ) on the walls of the lateral ventricle and the subgranular zone (SGZ) of the dentate gyrus (DG). However, the majority of newborn neurons undergo programmed cell death (PCD) during the period of proliferation, migration, and integration. Stroke activates neural stem cells (NSCs) in both SVZ and SGZ. This process is regulated by a wide variety of signaling pathways. However, the newborn neurons derived from adult neurogenesis are insufficient for tissue repair and function recovery. Thus, enhancing the endogenous neurogenesis driven by ischemia and promoting the survival of newborn neurons can be promising therapeutic interventions for stroke. Here, we present an overview of the process of adult neurogenesis and the potential of stroke-induced neurogenesis on brain repair.

scholarly journals Effects of Brain Size on Adult Neurogenesis in Shrews

2021 ◽  
Vol 22 (14) ◽  
pp. 7664
Author(s):  
Katarzyna Bartkowska ◽  
Krzysztof Turlejski ◽  
Beata Tepper ◽  
Leszek Rychlik ◽  
Peter Vogel ◽  
...  
Keyword(s):  
Adult Neurogenesis ◽  
Subventricular Zone ◽  
Molecular Mechanisms ◽  
Brain Size ◽  
Hippocampal Formation ◽  
Small Animals ◽  
Suncus Murinus ◽  
The Brain ◽  
Neomys Fodiens ◽  
Migratory Stream

Shrews are small animals found in many different habitats. Like other mammals, adult neurogenesis occurs in the subventricular zone of the lateral ventricle (SVZ) and the dentate gyrus (DG) of the hippocampal formation. We asked whether the number of new generated cells in shrews depends on their brain size. We examined Crocidura russula and Neomys fodiens, weighing 10–22 g, and Crocidura olivieri and Suncus murinus that weigh three times more. We found that the density of proliferated cells in the SVZ was approximately at the same level in all species. These cells migrated from the SVZ through the rostral migratory stream to the olfactory bulb (OB). In this pathway, a low level of neurogenesis occurred in C. olivieri compared to three other species of shrews. In the DG, the rate of adult neurogenesis was regulated differently. Specifically, the lowest density of newly generated neurons was observed in C. russula, which had a substantial number of new neurons in the OB compared with C. olivieri. We suggest that the number of newly generated neurons in an adult shrew’s brain is independent of the brain size, and molecular mechanisms of neurogenesis appeared to be different in two neurogenic structures.

scholarly journals miR-124 regulates adult neurogenesis in the subventricular zone stem cell niche

2009 ◽  
Vol 12 (4) ◽  
pp. 399-408 ◽  
Author(s):  
Li-Chun Cheng ◽  
Erika Pastrana ◽  
Masoud Tavazoie ◽  
Fiona Doetsch
Keyword(s):  
Stem Cell ◽  
Adult Neurogenesis ◽  
Subventricular Zone ◽  
Stem Cell Niche ◽  
Cell Niche

scholarly journals Single-Cell Transcriptomics Characterizes Cell Types in the Subventricular Zone and Uncovers Molecular Defects Impairing Adult Neurogenesis

Cell Reports ◽  
2018 ◽  
Vol 25 (9) ◽  
pp. 2457-2469.e8 ◽  
Author(s):  
Vera Zywitza ◽  
Aristotelis Misios ◽  
Lena Bunatyan ◽  
Thomas E. Willnow ◽  
Nikolaus Rajewsky
Keyword(s):  
Single Cell ◽  
Adult Neurogenesis ◽  
Subventricular Zone ◽  
Cell Types ◽  
Molecular Defects

scholarly journals TAZ Represses the Neuronal Commitment of Neural Stem Cells

Cells ◽  
2020 ◽  
Vol 9 (10) ◽  
pp. 2230
Author(s):  
Natalia Robledinos-Antón ◽  
Maribel Escoll ◽  
Kun-Liang Guan ◽  
Antonio Cuadrado
Keyword(s):  
Neuronal Differentiation ◽  
Subventricular Zone ◽  
Transcriptional Repression ◽  
Genetic Manipulation ◽  
Mammalian Brain ◽  
Additional Function ◽  
Neural Stem Progenitor Cells ◽  
Neuronal Lineage ◽  
Neuronal Commitment

The mechanisms involved in regulation of quiescence, proliferation, and reprogramming of Neural Stem Progenitor Cells (NSPCs) of the mammalian brain are still poorly defined. Here, we studied the role of the transcriptional co-factor TAZ, regulated by the WNT and Hippo pathways, in the homeostasis of NSPCs. We found that, in the murine neurogenic niches of the striatal subventricular zone and the dentate gyrus granular zone, TAZ is highly expressed in NSPCs and declines with ageing. Moreover, TAZ expression is lost in immature neurons of both neurogenic regions. To characterize mechanistically the role of TAZ in neuronal differentiation, we used the midbrain-derived NSPC line ReNcell VM to replicate in a non-animal model the factors influencing NSPC differentiation to the neuronal lineage. TAZ knock-down and forced expression in NSPCs led to increased and reduced neuronal differentiation, respectively. TEADs-knockdown indicated that these TAZ co-partners are required for the suppression of NSPCs commitment to neuronal differentiation. Genetic manipulation of the TAZ/TEAD system showed its participation in transcriptional repression of SOX2 and the proneuronal genes ASCL1, NEUROG2, and NEUROD1, leading to impediment of neurogenesis. TAZ is usually considered a transcriptional co-activator promoting stem cell proliferation, but our study indicates an additional function as a repressor of neuronal differentiation.

scholarly journals Syndecan-1 Stimulates Adult Neurogenesis in the Mouse Ventricular-Subventricular Zone after Injury

iScience ◽  
2020 ◽  
Vol 23 (12) ◽  
pp. 101784
Author(s):  
Marc-André Mouthon ◽  
Lise Morizur ◽  
Léa Dutour ◽  
Donovan Pineau ◽  
Thierry Kortulewski ◽  
...  
Keyword(s):  
Adult Neurogenesis ◽  
Subventricular Zone

scholarly journals Interaction between Angiotensin Type 1, Type 2, and Mas Receptors to Regulate Adult Neurogenesis in the Brain Ventricular–Subventricular Zone

Cells ◽  
2019 ◽  
Vol 8 (12) ◽  
pp. 1551 ◽  
Author(s):  
Maria Garcia-Garrote ◽  
Ana Perez-Villalba ◽  
Pablo Garrido-Gil ◽  
German Belenguer ◽  
Juan A. Parga ◽  
...  
Keyword(s):  
Adult Neurogenesis ◽  
Subventricular Zone ◽  
Functional Dependence ◽  
Renin Angiotensin System ◽  
At1 Receptor ◽  
Receptor Expression ◽  
At2 Receptor ◽  
Angiotensin Type

The renin–angiotensin system (RAS), and particularly its angiotensin type-2 receptors (AT2), have been classically involved in processes of cell proliferation and maturation during development. However, the potential role of RAS in adult neurogenesis in the ventricular-subventricular zone (V-SVZ) and its aging-related alterations have not been investigated. In the present study, we analyzed the role of major RAS receptors on neurogenesis in the V-SVZ of adult mice and rats. In mice, we showed that the increase in proliferation of cells in this neurogenic niche was induced by activation of AT2 receptors but depended partially on the AT2-dependent antagonism of AT1 receptor expression, which restricted proliferation. Furthermore, we observed a functional dependence of AT2 receptor actions on Mas receptors. In rats, where the levels of the AT1 relative to those of AT2 receptor are much lower, pharmacological inhibition of the AT1 receptor alone was sufficient in increasing AT2 receptor levels and proliferation in the V-SVZ. Our data revealed that interactions between RAS receptors play a major role in the regulation of V-SVZ neurogenesis, particularly in proliferation, generation of neuroblasts, and migration to the olfactory bulb, both in young and aged brains, and suggest potential beneficial effects of RAS modulators on neurogenesis.

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