Abstract
Adult neurogenesis represents a mature brain’s capacity to integrate newly generated neurons into functional circuits. Impairment of neurogenesis contributes to the pathophysiology of various mood and cognitive disorders such as depression and Alzheimer’s Disease. The hippocampal neurogenic niche hosts neural progenitors, glia, and vasculature, which all respond to intrinsic and environmental cues, helping determine their current state and ultimate fate. In this article we focus on the major immune communication pathways and mechanisms through which glial cells sense, interact with, and modulate the neurogenic niche. We pay particular attention to those related to the sensing of and response to innate immune danger signals. Receptors for danger signals were first discovered as a critical component of the innate immune system response to pathogens but are now also recognized to play a crucial role in modulating non-pathogenic sterile inflammation. In the neurogenic niche, viable, stressed, apoptotic, and dying cells can activate danger responses in neuroimmune cells, resulting in neuroprotection or neurotoxicity. Through these mechanisms glial cells can influence hippocampal stem cell fate, survival, neuronal maturation, and integration. Depending on the context, such responses may be appropriate and on-target, as in the case of learning-associated synaptic pruning, or excessive and off-target, as in neurodegenerative disorders.
Highlights
Adult mammalian brains preserve the capacity to generate and integrate new functional neurons through a process called adult neurogenesis
Adult neurogenesis has been demonstrated in the neurogenic niches of the subventricular zone (SVZ) of the lateral ventricles and the subgranular zone (SGZ)
Adult Hippocampal Neurogenesis (AHN) arises from the dichotomous differentiation potential of multipotent neural stem cells (NSCs) to self-renew and generate mature neurons that incorporate into the local hippocampal functional circuitry [8,9], or glia such as astrocytes (GFAP+S100β+) and oligodendrocytes in a process termed gliogenesis [10,11,12,13]
Summary
Adult mammalian brains preserve the capacity to generate and integrate new functional neurons through a process called adult neurogenesis. Recent evidence suggests that human brains can generate new neurons into very old age, even in individuals with marked cognitive impairment [6,7]. Neural stem and progenitor cells (NSCs, NPCs, respectively), are tasked with the generation of all new neurons, astrocytes, and oligodendrocytes. The fates of these stem/progenitor cells are determined by cell-intrinsic programming and signaling from their complex microenvironment. We will focus on how these cells are guided by danger and damage signals to help guide the fates of hippocampal progenitors and newborn neurons. Danger signaling provides an apt framework to explore how cell–cell and cell–environment interactions can shape neurogenesis and how these mechanisms might be exploited as part of future therapy development
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