Anti-inflammatory potential of thymosin β4 in the central nervous system: implications for progressive neurodegenerative diseases

Pardon, Marie-Christine

Abstract

Introduction: The actin-sequestering thymosin beta4 (Tβ4) is the most abundant member of the β-thymosins, and is widely expressed in the central nervous system (CNS), but its functions in the healthy and diseased brain are poorly understood. The expression of Tβ4 in neurons and microglia, the resident immune cells of the brain, suggests that it can play a role in modulating behavioral processes and immunological mechanisms in the brain. The purpose of this review is to shed lights on the role of Tβ4 in CNS function and diseases without antecedent autoimmune inflammation or injury, and to question its therapeutic potential for neurodegenerative disorders such as Alzheimer’s disease. Areas covered: This review presents the evidence supporting a role for Tβ4 in behaviors that are affected in CNS disorders, as well as studies linking Tβ4 upregulation in microglia to neuroinflammatory processes associated with these disorders. Finally, the implication of Tβ4 in the process of microglial activation and the mechanisms underlying its ability to suppress pro-inflammatory signaling in microglia are discussed. Expert opinion: Tβ4 has the potential to control inflammatory processes in the brain, opening avenues for new therapeutic applications to a range of neurodegenerative conditions.

Citation

Pardon, M.-C. (2018). Anti-inflammatory potential of thymosin β4 in the central nervous system: implications for progressive neurodegenerative diseases. Expert Opinion on Biological Therapy, 18(sup1), 165-169. https://doi.org/10.1080/14712598.2018.1486817

• Journal Article Type: Article
• Acceptance Date: Jun 6, 2018
• Online Publication Date: Jul 31, 2018
• Publication Date: 2018
• Deposit Date: Apr 30, 2019
• Journal: Expert Opinion on Biological Therapy
• Print ISSN: 1471-2598
• Electronic ISSN: 1744-7682
• Publisher: Taylor and Francis
• Peer Reviewed: Peer Reviewed
• Volume: 18
• Issue: sup1
• Pages: 165-169
• DOI: https://doi.org/10.1080/14712598.2018.1486817
• Public URL: https://nottingham-repository.worktribe.com/output/1860919
• Publisher URL: https://www.tandfonline.com/doi/abs/10.1080/14712598.2018.1486817?journalCode=iebt20
• Additional Information: Peer Review Statement: The publishing and review policy for this title is described in its Aims & Scope.; Aim & Scope: http://www.tandfonline.com/action/journalInformation?show=aimsScope&journalCode=iebt20