Abstract
In adult brain, new neurons are generated throughout adulthood in the subventricular zone and the dentate gyrus; this process is commonly known as adult neurogenesis. The regulation or modulation of adult neurogenesis includes various intrinsic pathways (signal transduction pathway and epigenetic or genetic modulation pathways) or extrinsic pathways (metabolic growth factor modulation, vascular, and immune system pathways). Altered neurogenesis has been identified in Alzheimer’s disease (AD), in both human AD brains and AD rodent models. The exact mechanism of the dysregulation of adult neurogenesis in AD has not been completely elucidated. However, neuroinflammation has been demonstrated to alter adult neurogenesis. The presence of various inflammatory components, such as immune cells, cytokines, or chemokines, plays a role in regulating the survival, proliferation, and maturation of neural stem cells. Neuroinflammation has also been considered as a hallmark neuropathological feature of AD. In this review, we summarize current, state-of-the art perspectives on adult neurogenesis, neuroinflammation, and the relationship between these two phenomena in AD. Furthermore, we discuss the potential therapeutic approaches, focusing on the anti-inflammatory and proneurogenic interventions that have been reported in this field.
Highlights
Alzheimer’s disease (AD) is the most common neurodegenerative dementia worldwide and is characterized by early impairment of recent memory
Adult neurogenesis in the mammalian brain has only been detected in certain limited regions, i.e., the subventricular zone (SVZ) and the subgranular zone (SGZ) of the hippocampus [48]
Due to the interconnection between neuroinflammation and neurodegeneration in AD, in this review, we summarize the current evidence regarding the impact of neuroinflammation on Adult hippocampal neurogenesis (AHN) and its relevance to AD
Summary
Alzheimer’s disease (AD) is the most common neurodegenerative dementia worldwide and is characterized by early impairment of recent memory. A number of studies have discussed the potential role of microglial genes in the regulation of neuroinflammation and the relationship between microglial genes and late-onset sporadic AD [29,37,38,39,40,41] This neuroinflammatory process is responsive to neuronal loss or to the presence of pathological protein aggregation in AD. Adult neurogenesis in the mammalian brain has only been detected in certain limited regions, i.e., the subventricular zone (SVZ) and the subgranular zone (SGZ) of the hippocampus [48]. These regions maintain a neurogenic stem cell niche. We discuss the potential therapeutic strategies regarding this issue
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