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Review
. 2020 Jan 21;21(3):701.
doi: 10.3390/ijms21030701.

Neuroinflammation and Neurogenesis in Alzheimer's Disease and Potential Therapeutic Approaches

Pi-Shan Sung  1   2 , Po-Yu Lin  1 , Chi-Hung Liu  3   4 , Hui-Chen Su  1 , Kuen-Jer Tsai  2   5
Affiliations
Review

Neuroinflammation and Neurogenesis in Alzheimer's Disease and Potential Therapeutic Approaches

Pi-Shan Sung et al. Int J Mol Sci. .

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.

Keywords: Alzheimer’s disease; neurogenesis; neuroinflammation.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
The potential therapeutic approaches targeting adult neurogenesis and inflammation in AD. PUFA, poly-unsaturated fatty acids; NSAID, nonsteroidal anti-inflammatory drugs; and LV-Wnt3, lentivirus expressing the WNT3 protein.
See this image and copyright information in PMC

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