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

被引：1

作者：

Aghajanov, M. I. ^{[1
]}

Harutyunyan, H. S. ^{[1
,2
]}

Khamperyan, A. Kh. ^{[2
]}

Karapetyan, G. A. ^{[2
]}

Fereshetyan, K. S. ^{[1
,2
]}

Yenkoyan, K. B. ^{[1
,2
,3
]}

机构：

[1] Yerevan State Med Univ, Dept Biochem, Yerevan, Armenia

[2] Yerevan State Med Univ, COBRAIN Ctr, Neurosci Lab, Yerevan, Armenia

[3] Yerevan State Med Univ, COBRAIN Ctr, Neurosci Lab, 2 Koryun, Yerevan 0025, Armenia

来源：

NEUROCHEMICAL JOURNAL | 2023年 / 17卷 / 04期

关键词：

ferroptosis; oxidative stress; Alzheimer's disease; experimental models; FAB model; GLUTATHIONE-PEROXIDASE; 4; BETA-AMYLOID PROTEIN; OXIDATIVE STRESS; LIPID-PEROXIDATION; IRON ACCUMULATION; CELL-DEATH; BRAIN; NEURODEGENERATION; NEURONS; DEFERIPRONE;

D O I：

10.1134/S1819712423040049

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

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.

引用

页码：608 / 617

页数：10