AGEs/RAGE-Related Neurodegeneration: daf-16 as a Mediator, Insulin as an Ameliorant, and C. elegans as an Expedient Research Model

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Abstract

Advanced glycation end-products (AGEs) are nonenzymatically glycated proteins, lipids, and nucleic acids. These compounds both originate exogenously and are formed endogenously, and they are associated, along with one of their receptors (RAGE), with a variety of pathologies and neurodegeneration. Some of their deleterious effects include affecting insulin signaling and FOXO-related pathways in both receptor-dependent and -independent manners. A potential ameliorating agent for these effects is insulin, which is being studied in several in vivo and in vitro models; one of these models is C. elegans, whose maintenance, genetic malleability, and well-described longevity-related pathways make it an optimal complementary model for assessing these objectives. In the realm of neuroscience, this model is currently being used only for general assessment of neurodegeneration and shortened lifespan. We suggest that characterization of (a) the effects of AGEs/RAGE on specific neurotransmitter systems, (b) the role of the daf-2/daf-16 pathway in these neurodegenerative processes, and

Original languageEnglish (US)
Pages (from-to)38-42
Number of pages5
JournalChemical Research in Toxicology
Volume30
Issue number1
DOIs
StatePublished - Jan 17 2017

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Advanced Glycosylation End Products
Insulin
Neurosciences
Research
Nucleic Acids
Neurotransmitter Agents
Maintenance
Pathology
Lipids
Proteins
In Vitro Techniques

ASJC Scopus subject areas

  • Toxicology

Cite this

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title = "AGEs/RAGE-Related Neurodegeneration: daf-16 as a Mediator, Insulin as an Ameliorant, and C. elegans as an Expedient Research Model",
abstract = "Advanced glycation end-products (AGEs) are nonenzymatically glycated proteins, lipids, and nucleic acids. These compounds both originate exogenously and are formed endogenously, and they are associated, along with one of their receptors (RAGE), with a variety of pathologies and neurodegeneration. Some of their deleterious effects include affecting insulin signaling and FOXO-related pathways in both receptor-dependent and -independent manners. A potential ameliorating agent for these effects is insulin, which is being studied in several in vivo and in vitro models; one of these models is C. elegans, whose maintenance, genetic malleability, and well-described longevity-related pathways make it an optimal complementary model for assessing these objectives. In the realm of neuroscience, this model is currently being used only for general assessment of neurodegeneration and shortened lifespan. We suggest that characterization of (a) the effects of AGEs/RAGE on specific neurotransmitter systems, (b) the role of the daf-2/daf-16 pathway in these neurodegenerative processes, and",
author = "Adi Pinkas and Michael Aschner",
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T2 - daf-16 as a Mediator, Insulin as an Ameliorant, and C. elegans as an Expedient Research Model

AU - Pinkas, Adi

AU - Aschner, Michael

PY - 2017/1/17

Y1 - 2017/1/17

N2 - Advanced glycation end-products (AGEs) are nonenzymatically glycated proteins, lipids, and nucleic acids. These compounds both originate exogenously and are formed endogenously, and they are associated, along with one of their receptors (RAGE), with a variety of pathologies and neurodegeneration. Some of their deleterious effects include affecting insulin signaling and FOXO-related pathways in both receptor-dependent and -independent manners. A potential ameliorating agent for these effects is insulin, which is being studied in several in vivo and in vitro models; one of these models is C. elegans, whose maintenance, genetic malleability, and well-described longevity-related pathways make it an optimal complementary model for assessing these objectives. In the realm of neuroscience, this model is currently being used only for general assessment of neurodegeneration and shortened lifespan. We suggest that characterization of (a) the effects of AGEs/RAGE on specific neurotransmitter systems, (b) the role of the daf-2/daf-16 pathway in these neurodegenerative processes, and

AB - Advanced glycation end-products (AGEs) are nonenzymatically glycated proteins, lipids, and nucleic acids. These compounds both originate exogenously and are formed endogenously, and they are associated, along with one of their receptors (RAGE), with a variety of pathologies and neurodegeneration. Some of their deleterious effects include affecting insulin signaling and FOXO-related pathways in both receptor-dependent and -independent manners. A potential ameliorating agent for these effects is insulin, which is being studied in several in vivo and in vitro models; one of these models is C. elegans, whose maintenance, genetic malleability, and well-described longevity-related pathways make it an optimal complementary model for assessing these objectives. In the realm of neuroscience, this model is currently being used only for general assessment of neurodegeneration and shortened lifespan. We suggest that characterization of (a) the effects of AGEs/RAGE on specific neurotransmitter systems, (b) the role of the daf-2/daf-16 pathway in these neurodegenerative processes, and

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