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Stroke, trauma and neurodegenerative diseases such as Alzheimer’s and Parkinson’s diseases affect millions of people worldwide. To date, treatment for these disorders is mainly symptomatic. However, the discovery of multipotent neural progenitor cell (NPC) capable of producing not only glia but also neurons in the adult brain has brought revolutionary changes in the field of restorative therapy. Currently, it posits that regeneration of neurons can occur throughout life, opening a door for the development of novel therapies to treat neurological diseases by neuronal regeneration using proliferation, differentiation, and integration of NPC at sites of brain injury. To achieve this goal, we need to strive to better understand the molecular signals involved in the control of NPC fate and the mechanisms inducing their migration and integration into the existing neural networks and synaptic circuits. The functional properties of the newborn neurons and their ability to form appropriate afferent and efferent connections should be determined for optimizing functional recovery in human disorders. In studying adult neurogenesis and adult NPC, the availability of developmental paradigms, such as embryonic neurogenesis and embryonic NPC, stands as a candidate experimental model. During the assembly of neural circuits in the developing brain, embryonic NPC generates functionally distinct neuronal cell types, each at a stereotyped position. In recent years, considerable progress has been made in defining the molecular players controlling embryonic NPC specification [1, 2]. These studies have revealed that neural cell fate depends critically on local environmental signals, which direct cell fates by inducing the expression of intrinsic proteins, notably transcription factors (TFs). In molecular biology, a TF is a protein that regulates transcription of target genes. In particular, TFs regulate the binding of RNA polymerase and the initiation of transcription. TFs act in networks [3] to induce the expression of target genes, which subsequently define the fate of the descendant cells (Fig. 1). In fact, developmental mechanisms may be more than just a model for studying the molecular regulation of adult neurogenesis. Recent laboratory evidence has identified some key embryonic NPC molecular regulators, such as sonic hedgehog and Wnt, as modulators of adult NPC [4–6]. In addition to these secreted signals, some of the intracellular TFs involved in developmental neural patterning were found to be expressed by and to affect aspects of the adult NPC biology (see [7] for a recent review). It is not surprising then that there is an increasing interest on how to employ TFs to manipulate endogenous NPC for the purposes of repairing the injured brain. In the current issue, Scholzke and Schwaninger [8] summarize the present state-of-the-art investigation on the TF involvement in neurogenesis after cerebral ischemia— the most common type of cerebral injury. Their review is unique, as it represents the first attempt to collectively analyze the transcriptional control of adult NPC in the context of reactive neurogenesis after ischemic damage to the brain. At present, the evidence for TF involvement in ischemia-induced adult neurogenesis is rather scarce and reports mainly the association of a certain TF with this process rather than its precise role. To overcome this, the authors review the major molecular players regulating embryonic NPC and then elegantly draw possible J Mol Med DOI 10.1007/s00109-007-0210-5

“Transcribing” postischemic neurogenesis: a tale revealing hopes of adult brain repair