Preface

**Section 3 Neurotrophin and Neuronal Fate Decision 179**

Chapter 7 **Neurotrophin Signaling and Alzheimer's Disease**

Chapter 8 **NFκB Signaling Directs Neuronal Fate Decision 197**

Chapter 9 **Telencephalic Neurogenesis Versus Telencephalic**

Chapter 11 **Neural Stem/Progenitor Cells for Spinal Cord**

**Embryonic Stem Cells 305** Atsushi Shimomura and Eri Hashino

Chapter 12 **Epigenetic Regulation of Neural Differentiation from**

**Differentiation of Pluripotent Stem Cells 217** Roxana Nat, Galina Apostolova and Georg Dechant

Chapter 10 **Regulation of Basal and Injury-Induced Fate Decisions of Adult**

Harleen S. Basrai, Kimberly J. Christie and Ann M. Turnley

Ryan Salewski, Hamideh Emrani and Michael G. Fehlings

Chapter 13 **Neural Fate of Mesenchymal Stem Cells and Neural Crest Stem Cells: Which Ways to Get Neurons for Cell Therapy**

Virginie Neirinckx, Cécile Coste, Bernard Rogister and Sabine Wislet-

**Neural Precursor Cells: Focus on SOCS2 and Related Signalling**

**Section 4 NF-K-b and Neuronal Fate Decision 195**

Yonggang Zhang and Wenhui Hu

**Section 5 Stem Cells and Signaling Pathways 215**

Jenny Wong

**VI** Contents

**Pathways 241**

**Regeneration 271**

**Purpose? 327**

Gendebien

**Neurodegeneration − Focus on BDNF/TrkB Signaling 181**

During the last decades, numerous studies about stem cells and regenerative medicine high‐ lighted new therapeutic approaches to treat several neurological disorders. It is noteworthy that the current optimism over potential stem cell therapies is driven by new understand‐ ings of stem cell biolology leading to specific cell fate decision.

The main objective of this book is to offer a general understanding of signaling pathways underlying the capacity of differentiation of several types of stem cells into neurons, during the development. Indeed, in this book, we deeply described TGF-beta signaling, Wnt Signal‐ ing, neurotrophin and NF-κ-B signaling and their implication in neuronal fate decision.

The second objective of this book is to understand how those pathways are altered in pathologi‐ cal conditions. We consequently analyzed those pathways in several pathological conditions.

Finally the third objective of this book is to describe advances in cellular therapy that could be use to restore central nervous system dysfunction in pathological conditions, based on new molecular biology findings. Several sources of stem cells and their potential benefits were described in the last part of this book.

Finally, I would like to conclude this preface by expressing my deepest gratitude to all au‐ thors who contributed to the elaboration of this book.

> **Sabine Wislet-Gendebien, PhD** GIGA Neurosciences University of Liège, Belgium

**Section 1**

**TGF-Beta Signaling and Neuronal Fate Decision**

**TGF-Beta Signaling and Neuronal Fate Decision**

**Chapter 1**

**Role of TGF-β Signaling in**

http://dx.doi.org/10.5772/53941

hippocampal dentate gyrus (DG) [2].

**1. Introduction**

**Neurogenic Regions After Brain Injury**

Sonia Villapol, Trevor T. Logan and Aviva J. Symes

In 1928 Santiago Ramón y Cajal penned what became the accepted view about neurons in the central nervous system*; "everything may die, nothing can be regenerated"*. He later exhibited his wisdom by adding; *"It's the job of science to rewrite, if possible, this cruel phrase"* [1]. Up until 20 years ago, the scientific literature had emphasized that neurogenesis only occurs during development with no new neurons generated in the adult mammalian brain. However, since the discovery of adult neurogenesis, an extensive literature has emerged supporting the constant generation of new neurons in two neurogenic regions of the adult brain: the subven‐ tricular zone around the lateral ventricles (SVZ) and the subgranular zone (SGZ) of the

The existence of adult neurogenesis gave hope for recovery and regeneration from the many different insults that can damage the brain. After stroke or traumatic brain injury (TBI), immediate massive necrosis occurs followed by a subsequent prolonged period of inflamma‐ tion and further neuronal death [3]. Although brain injury induces massive cell loss, it also induces an increase in proliferation of NSCs residing in the neurogenic niches [4]. The environment of the neurogenic niche in adult animals is exquisitely regulated, with a finelytuned balance of soluble and cell-intrinsic factors that regulate the many different processes that are critical to neurogenesis: cell survival, proliferation, differentiation, and migration [5]. Dramatic changes occur in this environment as a consequence of the injury. The careful regulation of neurogenesis is disrupted by the many different cellular, soluble and vascular signals detected by the different cell types in the SVZ and DG. This major environmental alteration leads to increased proliferation of progenitor cells for long periods after the acute injury, yet the ability of the neural progenitor cells to fully differentiate, migrate and integrate into the lesioned area is limited [6]. Understanding the signals that regulate adult neurogenesis

> © 2013 Villapol et al.; licensee InTech. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

© 2013 Villapol et al.; licensee InTech. This is a paper distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Additional information is available at the end of the chapter
