Iron Homeostasis Disorder and Alzheimer’s Disease
Iron is an essential trace metal for almost all organisms, including human; however, oxidative stress can easily be caused when iron is in excess, producing toxicity to the human body due to its capability to be both an electron donor and an electron acceptor. Although there is a strict regulation m...
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Published in | International journal of molecular sciences Vol. 22; no. 22; p. 12442 |
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Language | English |
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18.11.2021
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Abstract | Iron is an essential trace metal for almost all organisms, including human; however, oxidative stress can easily be caused when iron is in excess, producing toxicity to the human body due to its capability to be both an electron donor and an electron acceptor. Although there is a strict regulation mechanism for iron homeostasis in the human body and brain, it is usually inevitably disturbed by genetic and environmental factors, or disordered with aging, which leads to iron metabolism diseases, including many neurodegenerative diseases such as Alzheimer’s disease (AD). AD is one of the most common degenerative diseases of the central nervous system (CNS) threatening human health. However, the precise pathogenesis of AD is still unclear, which seriously restricts the design of interventions and treatment drugs based on the pathogenesis of AD. Many studies have observed abnormal iron accumulation in different regions of the AD brain, resulting in cognitive, memory, motor and other nerve damages. Understanding the metabolic balance mechanism of iron in the brain is crucial for the treatment of AD, which would provide new cures for the disease. This paper reviews the recent progress in the relationship between iron and AD from the aspects of iron absorption in intestinal cells, storage and regulation of iron in cells and organs, especially for the regulation of iron homeostasis in the human brain and prospects the future directions for AD treatments. |
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AbstractList | Iron is an essential trace metal for almost all organisms, including human; however, oxidative stress can easily be caused when iron is in excess, producing toxicity to the human body due to its capability to be both an electron donor and an electron acceptor. Although there is a strict regulation mechanism for iron homeostasis in the human body and brain, it is usually inevitably disturbed by genetic and environmental factors, or disordered with aging, which leads to iron metabolism diseases, including many neurodegenerative diseases such as Alzheimer's disease (AD). AD is one of the most common degenerative diseases of the central nervous system (CNS) threatening human health. However, the precise pathogenesis of AD is still unclear, which seriously restricts the design of interventions and treatment drugs based on the pathogenesis of AD. Many studies have observed abnormal iron accumulation in different regions of the AD brain, resulting in cognitive, memory, motor and other nerve damages. Understanding the metabolic balance mechanism of iron in the brain is crucial for the treatment of AD, which would provide new cures for the disease. This paper reviews the recent progress in the relationship between iron and AD from the aspects of iron absorption in intestinal cells, storage and regulation of iron in cells and organs, especially for the regulation of iron homeostasis in the human brain and prospects the future directions for AD treatments.Iron is an essential trace metal for almost all organisms, including human; however, oxidative stress can easily be caused when iron is in excess, producing toxicity to the human body due to its capability to be both an electron donor and an electron acceptor. Although there is a strict regulation mechanism for iron homeostasis in the human body and brain, it is usually inevitably disturbed by genetic and environmental factors, or disordered with aging, which leads to iron metabolism diseases, including many neurodegenerative diseases such as Alzheimer's disease (AD). AD is one of the most common degenerative diseases of the central nervous system (CNS) threatening human health. However, the precise pathogenesis of AD is still unclear, which seriously restricts the design of interventions and treatment drugs based on the pathogenesis of AD. Many studies have observed abnormal iron accumulation in different regions of the AD brain, resulting in cognitive, memory, motor and other nerve damages. Understanding the metabolic balance mechanism of iron in the brain is crucial for the treatment of AD, which would provide new cures for the disease. This paper reviews the recent progress in the relationship between iron and AD from the aspects of iron absorption in intestinal cells, storage and regulation of iron in cells and organs, especially for the regulation of iron homeostasis in the human brain and prospects the future directions for AD treatments. Iron is an essential trace metal for almost all organisms, including human; however, oxidative stress can easily be caused when iron is in excess, producing toxicity to the human body due to its capability to be both an electron donor and an electron acceptor. Although there is a strict regulation mechanism for iron homeostasis in the human body and brain, it is usually inevitably disturbed by genetic and environmental factors, or disordered with aging, which leads to iron metabolism diseases, including many neurodegenerative diseases such as Alzheimer’s disease (AD). AD is one of the most common degenerative diseases of the central nervous system (CNS) threatening human health. However, the precise pathogenesis of AD is still unclear, which seriously restricts the design of interventions and treatment drugs based on the pathogenesis of AD. Many studies have observed abnormal iron accumulation in different regions of the AD brain, resulting in cognitive, memory, motor and other nerve damages. Understanding the metabolic balance mechanism of iron in the brain is crucial for the treatment of AD, which would provide new cures for the disease. This paper reviews the recent progress in the relationship between iron and AD from the aspects of iron absorption in intestinal cells, storage and regulation of iron in cells and organs, especially for the regulation of iron homeostasis in the human brain and prospects the future directions for AD treatments. |
Author | Chang, Xuejiao Lang, Minglin Peng, Yu |
AuthorAffiliation | 1 CAS Center for Excellence in Biotic Interactions, College of Life Science, University of Chinese Academy of Sciences, Beijing 100049, China; pengyu18@mails.ucas.ac.cn (Y.P.); changxuejiao20@mails.ucas.ac.cn (X.C.) 2 College of Life Science, Agricultural University of Hebei, Baoding 071000, China |
AuthorAffiliation_xml | – name: 1 CAS Center for Excellence in Biotic Interactions, College of Life Science, University of Chinese Academy of Sciences, Beijing 100049, China; pengyu18@mails.ucas.ac.cn (Y.P.); changxuejiao20@mails.ucas.ac.cn (X.C.) – name: 2 College of Life Science, Agricultural University of Hebei, Baoding 071000, China |
Author_xml | – sequence: 1 givenname: Yu surname: Peng fullname: Peng, Yu – sequence: 2 givenname: Xuejiao surname: Chang fullname: Chang, Xuejiao – sequence: 3 givenname: Minglin orcidid: 0000-0003-3801-2675 surname: Lang fullname: Lang, Minglin |
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SubjectTerms | Alzheimer Disease - complications Alzheimer Disease - genetics Alzheimer Disease - metabolism Alzheimer Disease - pathology Alzheimer's disease Amyloid beta-Peptides - genetics Amyloid beta-Peptides - metabolism Antigens, CD - genetics Antigens, CD - metabolism Apoptosis Blood Brain - metabolism Brain - pathology Cation Transport Proteins - genetics Cation Transport Proteins - metabolism Chemical reactions Cytochrome Gene Expression Regulation Hepatocytes - metabolism Hepatocytes - pathology Homeostasis Homeostasis - genetics Human body Humans Intestinal Absorption Iron Iron - metabolism Iron Overload - complications Iron Overload - etiology Iron Overload - genetics Iron Overload - metabolism Liver - metabolism Liver - pathology Macrophages - metabolism Macrophages - pathology Metabolic disorders Oxidative stress Pathogenesis Physiology Plasma Proteins Receptors, Transferrin - genetics Receptors, Transferrin - metabolism Regulation Review Sulfur Transcription Factors - genetics Transcription Factors - metabolism Transferrin - genetics Transferrin - metabolism Transfusion Reaction - complications |
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