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Role of the Insulin-like Growth Factor System in Neurodegenerative Disease.

作者信息

Lewitt Moira S, Boyd Gary W

机构信息

School of Health and Life Sciences, University of the West of Scotland, Paisley PA1 2BE, UK.

School of Health and Life Sciences, University of the West of Scotland, Hamilton G72 0LH, UK.

出版信息

Int J Mol Sci. 2024 Apr 20;25(8):4512. doi: 10.3390/ijms25084512.


DOI:10.3390/ijms25084512
PMID:38674097
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11049992/
Abstract

The insulin-like growth factor (IGF) system has paracrine and endocrine roles in the central nervous system. There is evidence that IGF signalling pathways have roles in the pathophysiology of neurodegenerative disease. This review focusses on Alzheimer's disease and Parkinson's disease, the two most common neurodegenerative disorders that are increasing in prevalence globally in relation to the aging population and the increasing prevalence of obesity and type 2 diabetes. Rodent models used in the study of the molecular pathways involved in neurodegeneration are described. However, currently, no animal model fully replicates these diseases. Mice with triple mutations in , and show promise as models for the testing of novel Alzheimer's therapies. While a causal relationship is not proven, the fact that age, obesity and T2D are risk factors in both strengthens the case for the involvement of the IGF system in these disorders. The IGF system is an attractive target for new approaches to management; however, there are gaps in our understanding that first need to be addressed. These include a focus beyond IGF-I on other members of the IGF system, including IGF-II, IGF-binding proteins and the type 2 IGF receptor.

摘要
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2dd8/11049992/600e8bea5177/ijms-25-04512-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2dd8/11049992/c7a72791c231/ijms-25-04512-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2dd8/11049992/600e8bea5177/ijms-25-04512-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2dd8/11049992/c7a72791c231/ijms-25-04512-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2dd8/11049992/600e8bea5177/ijms-25-04512-g002.jpg

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引用本文的文献

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Int J Mol Sci. 2025-7-17

[2]
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[3]
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[4]
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Mol Med Rep. 2025-5

[5]
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Neural Regen Res. 2026-4-1

[6]
Retinal Inflammation and Reactive Müller Cells: Neurotrophins' Release and Neuroprotective Strategies.

Biology (Basel). 2024-12-9

本文引用的文献

[1]
Identification of IGF-1 Effects on White Adipose Tissue and Hippocampus in Alzheimer's Disease Mice via Transcriptomic and Cellular Analysis.

Int J Mol Sci. 2024-2-22

[2]
Updates on mouse models of Alzheimer's disease.

Mol Neurodegener. 2024-3-11

[3]
Considering Aging on a Temporal and Tissue Scale: The Case of Insulin/IGF-1 Signaling.

Cells. 2024-2-5

[4]
Alleviation of behavioral deficits, amyloid-β deposition, and mitochondrial structure damage associated with mitophagy upregulation in AD animal models via AAV9-IGF-1 treatment.

Brain Res. 2024-3-15

[5]
The Role of Insulin-like Growth Factor I in Mechanisms of Resilience and Vulnerability to Sporadic Alzheimer's Disease.

Int J Mol Sci. 2023-11-17

[6]
Effects of rasagiline combined with levodopa and benserazide hydrochloride on motor function and homocysteine and IGF-1 levels in elderly patients with Parkinson's disease.

BMC Neurol. 2023-10-6

[7]
Viktor Mutt lecture: Peptides can cross the blood-brain barrier.

Peptides. 2023-11

[8]
Repositioning of Anti-Diabetic Drugs against Dementia: Insight from Molecular Perspectives to Clinical Trials.

Int J Mol Sci. 2023-7-14

[9]
Potential Role of Glucagon-like Peptide-1 Receptor Agonists in the Treatment of Cognitive Decline and Dementia in Diabetes Mellitus.

Int J Mol Sci. 2023-7-11

[10]
Prenatal stress aggravates age-dependent cognitive decline, insulin signaling dysfunction, and the pro-inflammatory response in the APP mouse model of Alzheimer's disease.

Neurobiol Dis. 2023-8

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