Potential therapeutic targets for Alzheimer's disease: Fibroblast growth factors and their regulation of ferroptosis, pyroptosis and autophagy.

Abstract

Alzheimer's disease (AD) is a progressively worsening neurodegenerative disorder characterized primarily by the deposition of amyloid beta (Aβ) plaques in the brain and the abnormal aggregation of tau protein forming neurofibrillary tangles. These pathological changes lead to impaired neuronal function and cell death, subsequently affecting the structure and function of the brain. Fibroblast growth factors (FGFs) are a group of proteins that play crucial roles in various biological processes, including cell proliferation, differentiation, and survival. This article reviews the expression and regulation of FGFs in the central nervous system and how they affect neuronal survival, as well as the changes in FGF signaling pathways and its regulation of programmed cell death in AD. It particularly focuses on the impact of FGF1, FGF2, FGF21, other members of the FGF family, and FGFR on the pathophysiological mechanisms of AD. The potential of the PI3K/AKT/GSK-3β, Wnt/β-catenin, and NF-κB signaling pathways as targets for AD treatment is also discussed. Furthermore, the relationship between FGF-regulated ferroptosis, Pyroptosis and Autophagy and AD is explored, along with the role of these mechanisms in improving the progression of AD.