Targeting amyloid-beta by glucagon-like peptide -1 (GLP-1) in Alzheimer's disease and diabetes

Ann Mosegaard Bak; Lærke Egefjord; Michael Gejl; Charlotte Kahlen Steffensen; Chalotte Willemann Stecher; Kamille Smidt; Birgitte Brock; Jørgen Rungby

doi:10.1517/14728222.2011.600691

Targeting amyloid-beta by glucagon-like peptide -1 (GLP-1) in Alzheimer's disease and diabetes

Ann Mosegaard Bak, Lærke Egefjord, Michael Gejl, Charlotte Kahlen Steffensen, Chalotte Willemann Stecher, Kamille Smidt, Birgitte Brock, Jørgen Rungby

32 Citations (Scopus)

Abstract

INTRODUCTION: Epidemiological evidence suggests an association between type 2 diabetes (T2DM) and Alzheimer's disease (AD), in that one disease increases the risk of the other. T2DM and AD share several molecular processes which underlie the tissue degeneration in either disease. Disturbances in insulin signaling may be the link between the two conditions. Drugs originally developed for T2DM are currently being considered as possible novel agents in the treatment of AD.

AREAS COVERED: This review discusses the potential role of glucagon-like peptide -1 (GLP-1) treatment in AD. GLP-1 receptors are expressed in areas of the brain important to memory and learning, and GLP-1 has growth-factor-like properties similar to insulin. A key neuropathological feature of AD is the accumulation of amyloid-beta (Aβ). In preclinical studies, GLP-1 and longer lasting analogues have been shown to have both neuroprotective and neurotrophic effects, and to protect synaptic activity in the brain from Aβ toxicity.

EXPERT OPINION: A convincing amount of evidence has shown a beneficial effect of GLP-1 agonist treatment on cognitive function, memory and learning in experimental models of AD. GLP-1 analogues may therefore be the new therapeutic agent of choice for intervention in AD.

Original language	English
Journal	Expert Opinion on Therapeutic Targets
Volume	15
Issue number	10
Pages (from-to)	1153-62
Number of pages	10
ISSN	1472-8222
DOIs	https://doi.org/10.1517/14728222.2011.600691
Publication status	Published - Oct 2011
Externally published	Yes

Keywords

Alzheimer Disease
Amyloid beta-Peptides
Animals
Cognition
Diabetes Mellitus, Type 2
Glucagon-Like Peptide 1
Humans
Learning
Memory
Neuroprotective Agents
Rats
Journal Article
Review

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10.1517/14728222.2011.600691

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title = "Targeting amyloid-beta by glucagon-like peptide -1 (GLP-1) in Alzheimer's disease and diabetes",

abstract = "INTRODUCTION: Epidemiological evidence suggests an association between type 2 diabetes (T2DM) and Alzheimer's disease (AD), in that one disease increases the risk of the other. T2DM and AD share several molecular processes which underlie the tissue degeneration in either disease. Disturbances in insulin signaling may be the link between the two conditions. Drugs originally developed for T2DM are currently being considered as possible novel agents in the treatment of AD.AREAS COVERED: This review discusses the potential role of glucagon-like peptide -1 (GLP-1) treatment in AD. GLP-1 receptors are expressed in areas of the brain important to memory and learning, and GLP-1 has growth-factor-like properties similar to insulin. A key neuropathological feature of AD is the accumulation of amyloid-beta (Aβ). In preclinical studies, GLP-1 and longer lasting analogues have been shown to have both neuroprotective and neurotrophic effects, and to protect synaptic activity in the brain from Aβ toxicity.EXPERT OPINION: A convincing amount of evidence has shown a beneficial effect of GLP-1 agonist treatment on cognitive function, memory and learning in experimental models of AD. GLP-1 analogues may therefore be the new therapeutic agent of choice for intervention in AD.",

keywords = "Alzheimer Disease, Amyloid beta-Peptides, Animals, Cognition, Diabetes Mellitus, Type 2, Glucagon-Like Peptide 1, Humans, Learning, Memory, Neuroprotective Agents, Rats, Journal Article, Review",

author = "Bak, \{Ann Mosegaard\} and L{\ae}rke Egefjord and Michael Gejl and Steffensen, \{Charlotte Kahlen\} and Stecher, \{Chalotte Willemann\} and Kamille Smidt and Birgitte Brock and J{\o}rgen Rungby",

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AU - Bak, Ann Mosegaard

AU - Egefjord, Lærke

AU - Gejl, Michael

AU - Steffensen, Charlotte Kahlen

AU - Stecher, Chalotte Willemann

AU - Smidt, Kamille

AU - Brock, Birgitte

AU - Rungby, Jørgen

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N2 - INTRODUCTION: Epidemiological evidence suggests an association between type 2 diabetes (T2DM) and Alzheimer's disease (AD), in that one disease increases the risk of the other. T2DM and AD share several molecular processes which underlie the tissue degeneration in either disease. Disturbances in insulin signaling may be the link between the two conditions. Drugs originally developed for T2DM are currently being considered as possible novel agents in the treatment of AD.AREAS COVERED: This review discusses the potential role of glucagon-like peptide -1 (GLP-1) treatment in AD. GLP-1 receptors are expressed in areas of the brain important to memory and learning, and GLP-1 has growth-factor-like properties similar to insulin. A key neuropathological feature of AD is the accumulation of amyloid-beta (Aβ). In preclinical studies, GLP-1 and longer lasting analogues have been shown to have both neuroprotective and neurotrophic effects, and to protect synaptic activity in the brain from Aβ toxicity.EXPERT OPINION: A convincing amount of evidence has shown a beneficial effect of GLP-1 agonist treatment on cognitive function, memory and learning in experimental models of AD. GLP-1 analogues may therefore be the new therapeutic agent of choice for intervention in AD.

AB - INTRODUCTION: Epidemiological evidence suggests an association between type 2 diabetes (T2DM) and Alzheimer's disease (AD), in that one disease increases the risk of the other. T2DM and AD share several molecular processes which underlie the tissue degeneration in either disease. Disturbances in insulin signaling may be the link between the two conditions. Drugs originally developed for T2DM are currently being considered as possible novel agents in the treatment of AD.AREAS COVERED: This review discusses the potential role of glucagon-like peptide -1 (GLP-1) treatment in AD. GLP-1 receptors are expressed in areas of the brain important to memory and learning, and GLP-1 has growth-factor-like properties similar to insulin. A key neuropathological feature of AD is the accumulation of amyloid-beta (Aβ). In preclinical studies, GLP-1 and longer lasting analogues have been shown to have both neuroprotective and neurotrophic effects, and to protect synaptic activity in the brain from Aβ toxicity.EXPERT OPINION: A convincing amount of evidence has shown a beneficial effect of GLP-1 agonist treatment on cognitive function, memory and learning in experimental models of AD. GLP-1 analogues may therefore be the new therapeutic agent of choice for intervention in AD.

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KW - Diabetes Mellitus, Type 2

KW - Glucagon-Like Peptide 1

KW - Humans

KW - Learning

KW - Memory

KW - Neuroprotective Agents

KW - Rats

KW - Journal Article

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Targeting amyloid-beta by glucagon-like peptide -1 (GLP-1) in Alzheimer's disease and diabetes

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Keywords

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