Ferroptosis in the Pathogenesis of Alzheimer’s Disease: The New Evidence for Validation of FAB Model

Pleiades Publishing Ltd - 2023
M. I. Aghajanov1, H. S. Harutyunyan1, Arpine Khamperyan2, G. A. Karapetyan2, Katarine Fereshetyan1, Konstantin Yenkoyan2
1Department of Biochemistry, Yerevan State Medical University Named after Mkhitar Heratsi, Yerevan, Armenia
2Neuroscience Laboratory, COBRAIN Center, Yerevan State Medical University Named after Mkhitar Heratsi, Yerevan, Armenia

Tóm tắt

Abstract Alzheimer’s disease is an age-associated progressive disorder, characterized by neurodegeneration and following cognitive decline. Several pathological alterations are implicated in its pathogenesis, hence etiology is still poorly understood. Ferroptosis is an alternative form of cell death, driven by intracellular accumulation of iron with subsequent reactive oxygen species formation, which damages membranes, proteins, and DNA, causing cell death. The imbalance in iron homeostasis is rapidly gaining weight as a neurodegeneration cause, increasing the need to develop in vivo and in vitro models to understand the role of ferroptosis in Alzheimer’s disease pathogenesis. This review focuses on the mechanisms of ferroptosis in the pathogenesis of AD, giving a detailed overview of the available in vivo and in vitro methods and their applications, as well as describing in detail the ferrous amyloid buthionine (FAB) model.

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