Roles for c-Abl in postoperative neurodegeneration

Abstract

The nonreceptor tyrosine kinase c-Abl is inactive under normal conditions. Upon activation, c-Abl regulates signaling pathways related to cytoskeletal reorganization. It plays a vital role in modulating cell protrusion, cell migration, morphogenesis, adhesion, endocytosis and phagocytosis. A large number of studies have also found that abnormally activated c-Abl plays an important role in a variety of pathologies, including various inflammatory diseases and neurodegenerative diseases. c-Abl also plays a crucial role in neurodevelopment and neurodegenerative diseases, mainly through mechanisms such as neuroinflammation, oxidative stress (OS), and Tau protein phosphorylation. Inhibiting expression or activity of this kinase has certain neuroprotective and anti-inflammatory effects and can also improve cognition and behavior. Blockers of this kinase may have good preventive and treatment effects on neurodegenerative diseases. Cognitive dysfunction after anesthesia is also closely related to the abovementioned mechanisms. We infer that alterations in the expression and activity of c-Abl may underlie postoperative cognitive dysfunction (POCD). This article summarizes the current understanding and research progress on the mechanisms by which c-Abl may be related to postoperative neurodegeneration.

Keywords: Alzheimer's disease; Nonreceptor tyrosine kinase; Oxidative stress; Parkinson's disease; Postoperative cognitive dysfunction; Postoperative neurodegeneration.

Figure 1

The current understanding and research progress on the mechanisms by which c-Abl may be related to neurodegenerative diseases.