TREM2 in the pathogenesis of AD: a lipid metabolism regulator and potential metabolic therapeutic target

Triggering receptor expressed on myeloid cells 2 (TREM2) is a single-pass transmembrane immune receptor that is mainly expressed on microglia in the brain and macrophages in the periphery. Recent studies have identified TREM2 as a risk factor for Alzheimer’s disease (AD). Increasing evidence has sho...

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Published inMolecular neurodegeneration Vol. 17; no. 1; pp. 40 - 19
Main Authors Li, Rui-Yang, Qin, Qi, Yang, Han-Chen, Wang, Ying-Ying, Mi, Ying-Xin, Yin, Yun-Si, Wang, Meng, Yu, Chao-Ji, Tang, Yi
Format Journal Article
LanguageEnglish
Published England BioMed Central Ltd 03.06.2022
BioMed Central
BMC
Subjects
Advertising executives
Alzheimer Disease - metabolism
Alzheimer's disease
Arteriosclerosis
Atherosclerosis
Blood-brain barrier
Brain - metabolism
Brain research
Central nervous system
Central Nervous System - pathology
Cholesterol
Cloning
Dementia
Enzymes
Fatty liver
Health aspects
Humans
Hypercholesterolemia
Insulin
Insulin resistance
Ligands
Lipid Metabolism
Lipids
Lipoproteins
Liver diseases
Macrophages
Medical research
Medicine, Experimental
Membrane Glycoproteins - metabolism
Metabolism
Microglia
Microglia - metabolism
Myelin
Myeloid cells
Neurodegenerative diseases
Pathogenesis
Peripheral system
Phenotypes
Phospholipids
Physiological aspects
Proteins
Receptors, Immunologic - metabolism
Review
Risk factors
Signal transduction
Target marketing
Therapeutic target
Therapeutic targets
TREM2
TREM2
Lipid metabolism
Alzheimer’s disease
Therapeutic target
Central nervous system
Peripheral system
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Abstract Triggering receptor expressed on myeloid cells 2 (TREM2) is a single-pass transmembrane immune receptor that is mainly expressed on microglia in the brain and macrophages in the periphery. Recent studies have identified TREM2 as a risk factor for Alzheimer’s disease (AD). Increasing evidence has shown that TREM2 can affect lipid metabolism both in the central nervous system (CNS) and in the periphery. In the CNS, TREM2 affects the metabolism of cholesterol, myelin, and phospholipids and promotes the transition of microglia into a disease-associated phenotype. In the periphery, TREM2 influences lipid metabolism by regulating the onset and progression of obesity and its complications, such as hypercholesterolemia, atherosclerosis, and nonalcoholic fatty liver disease. All these altered lipid metabolism processes could influence the pathogenesis of AD through several means, including affecting inflammation, insulin resistance, and AD pathologies. Herein, we will discuss a potential pathway that TREM2 mediates lipid metabolism to influence the pathogenesis of AD in both the CNS and periphery. Moreover, we discuss the possibility that TREM2 may be a key factor that links central and peripheral lipid metabolism under disease conditions, including AD. This link may be due to impacts on the integrity of the blood–brain barrier, and we introduce potential pathways by which TREM2 affects the blood–brain barrier. Moreover, we discuss the role of lipids in TREM2-associated treatments for AD. We propose some potential therapies targeting TREM2 and discuss the prospect and limitations of these therapies.
AbstractList Triggering receptor expressed on myeloid cells 2 (TREM2) is a single-pass transmembrane immune receptor that is mainly expressed on microglia in the brain and macrophages in the periphery. Recent studies have identified TREM2 as a risk factor for Alzheimer’s disease (AD). Increasing evidence has shown that TREM2 can affect lipid metabolism both in the central nervous system (CNS) and in the periphery. In the CNS, TREM2 affects the metabolism of cholesterol, myelin, and phospholipids and promotes the transition of microglia into a disease-associated phenotype. In the periphery, TREM2 influences lipid metabolism by regulating the onset and progression of obesity and its complications, such as hypercholesterolemia, atherosclerosis, and nonalcoholic fatty liver disease. All these altered lipid metabolism processes could influence the pathogenesis of AD through several means, including affecting inflammation, insulin resistance, and AD pathologies. Herein, we will discuss a potential pathway that TREM2 mediates lipid metabolism to influence the pathogenesis of AD in both the CNS and periphery. Moreover, we discuss the possibility that TREM2 may be a key factor that links central and peripheral lipid metabolism under disease conditions, including AD. This link may be due to impacts on the integrity of the blood–brain barrier, and we introduce potential pathways by which TREM2 affects the blood–brain barrier. Moreover, we discuss the role of lipids in TREM2-associated treatments for AD. We propose some potential therapies targeting TREM2 and discuss the prospect and limitations of these therapies.
Triggering receptor expressed on myeloid cells 2 (TREM2) is a single-pass transmembrane immune receptor that is mainly expressed on microglia in the brain and macrophages in the periphery. Recent studies have identified TREM2 as a risk factor for Alzheimer's disease (AD). Increasing evidence has shown that TREM2 can affect lipid metabolism both in the central nervous system (CNS) and in the periphery. In the CNS, TREM2 affects the metabolism of cholesterol, myelin, and phospholipids and promotes the transition of microglia into a disease-associated phenotype. In the periphery, TREM2 influences lipid metabolism by regulating the onset and progression of obesity and its complications, such as hypercholesterolemia, atherosclerosis, and nonalcoholic fatty liver disease. All these altered lipid metabolism processes could influence the pathogenesis of AD through several means, including affecting inflammation, insulin resistance, and AD pathologies. Herein, we will discuss a potential pathway that TREM2 mediates lipid metabolism to influence the pathogenesis of AD in both the CNS and periphery. Moreover, we discuss the possibility that TREM2 may be a key factor that links central and peripheral lipid metabolism under disease conditions, including AD. This link may be due to impacts on the integrity of the blood-brain barrier, and we introduce potential pathways by which TREM2 affects the blood-brain barrier. Moreover, we discuss the role of lipids in TREM2-associated treatments for AD. We propose some potential therapies targeting TREM2 and discuss the prospect and limitations of these therapies. Keywords: Alzheimer's disease, Central nervous system, Lipid metabolism, Peripheral system, Therapeutic target, TREM2
Abstract Triggering receptor expressed on myeloid cells 2 (TREM2) is a single-pass transmembrane immune receptor that is mainly expressed on microglia in the brain and macrophages in the periphery. Recent studies have identified TREM2 as a risk factor for Alzheimer’s disease (AD). Increasing evidence has shown that TREM2 can affect lipid metabolism both in the central nervous system (CNS) and in the periphery. In the CNS, TREM2 affects the metabolism of cholesterol, myelin, and phospholipids and promotes the transition of microglia into a disease-associated phenotype. In the periphery, TREM2 influences lipid metabolism by regulating the onset and progression of obesity and its complications, such as hypercholesterolemia, atherosclerosis, and nonalcoholic fatty liver disease. All these altered lipid metabolism processes could influence the pathogenesis of AD through several means, including affecting inflammation, insulin resistance, and AD pathologies. Herein, we will discuss a potential pathway that TREM2 mediates lipid metabolism to influence the pathogenesis of AD in both the CNS and periphery. Moreover, we discuss the possibility that TREM2 may be a key factor that links central and peripheral lipid metabolism under disease conditions, including AD. This link may be due to impacts on the integrity of the blood–brain barrier, and we introduce potential pathways by which TREM2 affects the blood–brain barrier. Moreover, we discuss the role of lipids in TREM2-associated treatments for AD. We propose some potential therapies targeting TREM2 and discuss the prospect and limitations of these therapies.
Triggering receptor expressed on myeloid cells 2 (TREM2) is a single-pass transmembrane immune receptor that is mainly expressed on microglia in the brain and macrophages in the periphery. Recent studies have identified TREM2 as a risk factor for Alzheimer's disease (AD). Increasing evidence has shown that TREM2 can affect lipid metabolism both in the central nervous system (CNS) and in the periphery. In the CNS, TREM2 affects the metabolism of cholesterol, myelin, and phospholipids and promotes the transition of microglia into a disease-associated phenotype. In the periphery, TREM2 influences lipid metabolism by regulating the onset and progression of obesity and its complications, such as hypercholesterolemia, atherosclerosis, and nonalcoholic fatty liver disease. All these altered lipid metabolism processes could influence the pathogenesis of AD through several means, including affecting inflammation, insulin resistance, and AD pathologies. Herein, we will discuss a potential pathway that TREM2 mediates lipid metabolism to influence the pathogenesis of AD in both the CNS and periphery. Moreover, we discuss the possibility that TREM2 may be a key factor that links central and peripheral lipid metabolism under disease conditions, including AD. This link may be due to impacts on the integrity of the blood-brain barrier, and we introduce potential pathways by which TREM2 affects the blood-brain barrier. Moreover, we discuss the role of lipids in TREM2-associated treatments for AD. We propose some potential therapies targeting TREM2 and discuss the prospect and limitations of these therapies.Triggering receptor expressed on myeloid cells 2 (TREM2) is a single-pass transmembrane immune receptor that is mainly expressed on microglia in the brain and macrophages in the periphery. Recent studies have identified TREM2 as a risk factor for Alzheimer's disease (AD). Increasing evidence has shown that TREM2 can affect lipid metabolism both in the central nervous system (CNS) and in the periphery. In the CNS, TREM2 affects the metabolism of cholesterol, myelin, and phospholipids and promotes the transition of microglia into a disease-associated phenotype. In the periphery, TREM2 influences lipid metabolism by regulating the onset and progression of obesity and its complications, such as hypercholesterolemia, atherosclerosis, and nonalcoholic fatty liver disease. All these altered lipid metabolism processes could influence the pathogenesis of AD through several means, including affecting inflammation, insulin resistance, and AD pathologies. Herein, we will discuss a potential pathway that TREM2 mediates lipid metabolism to influence the pathogenesis of AD in both the CNS and periphery. Moreover, we discuss the possibility that TREM2 may be a key factor that links central and peripheral lipid metabolism under disease conditions, including AD. This link may be due to impacts on the integrity of the blood-brain barrier, and we introduce potential pathways by which TREM2 affects the blood-brain barrier. Moreover, we discuss the role of lipids in TREM2-associated treatments for AD. We propose some potential therapies targeting TREM2 and discuss the prospect and limitations of these therapies.
ArticleNumber 40
Audience Academic
Author Yin, Yun-Si
Yu, Chao-Ji
Qin, Qi
Li, Rui-Yang
Wang, Meng
Yang, Han-Chen
Wang, Ying-Ying
Tang, Yi
Mi, Ying-Xin
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  fullname: Mi, Ying-Xin
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  surname: Wang
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  surname: Tang
  fullname: Tang, Yi
BackLink https://www.ncbi.nlm.nih.gov/pubmed/35658903$$D View this record in MEDLINE/PubMed
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Issue 1
Keywords TREM2
Lipid metabolism
Alzheimer’s disease
Therapeutic target
Central nervous system
Peripheral system
Language English
License 2022. The Author(s).
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Snippet Triggering receptor expressed on myeloid cells 2 (TREM2) is a single-pass transmembrane immune receptor that is mainly expressed on microglia in the brain and...
Abstract Triggering receptor expressed on myeloid cells 2 (TREM2) is a single-pass transmembrane immune receptor that is mainly expressed on microglia in the...
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StartPage 40
SubjectTerms Advertising executives
Alzheimer Disease - metabolism
Alzheimer's disease
Arteriosclerosis
Atherosclerosis
Blood-brain barrier
Brain - metabolism
Brain research
Central nervous system
Central Nervous System - pathology
Cholesterol
Cloning
Dementia
Enzymes
Fatty liver
Health aspects
Humans
Hypercholesterolemia
Insulin
Insulin resistance
Ligands
Lipid Metabolism
Lipids
Lipoproteins
Liver diseases
Macrophages
Medical research
Medicine, Experimental
Membrane Glycoproteins - metabolism
Metabolism
Microglia
Microglia - metabolism
Myelin
Myeloid cells
Neurodegenerative diseases
Pathogenesis
Peripheral system
Phenotypes
Phospholipids
Physiological aspects
Proteins
Receptors, Immunologic - metabolism
Review
Risk factors
Signal transduction
Target marketing
Therapeutic target
Therapeutic targets
TREM2
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Title TREM2 in the pathogenesis of AD: a lipid metabolism regulator and potential metabolic therapeutic target
URI https://www.ncbi.nlm.nih.gov/pubmed/35658903
https://www.proquest.com/docview/2678218757
https://www.proquest.com/docview/2673597195
https://pubmed.ncbi.nlm.nih.gov/PMC9166437
https://doaj.org/article/56afbf6988584e16b24e682bda671f1e
Volume 17
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