ArticleNeurochemical research2004
Generation of transgenic mice expressing insulin-like growth factor-1 under the control of the myelin basic protein promoter: increased myelination and potential for studies on the effects of increased IGF-1 on experimentally and genetically induced demyelination.
Article in Neurochemical research, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 22 citations in OpenAlex.
- Sex differences in the effects of high fat diet on underlying neuropathology in a mouse model of VCID.Biology of sex differences · 2023Article
- Hormonal Regulation of Oligodendrogenesis I: Effects across the Lifespan.Biomolecules · 2021Review
- Behavioral experiences as drivers of oligodendrocyte lineage dynamics and myelin plasticity.Neuropharmacology · 2016Review
- Promoting return of function in multiple sclerosis: An integrated approach.Multiple sclerosis and related disorders · 2013Article
- Signaling mechanisms regulating myelination in the central nervous system.Neuroscience bulletin · 2013Article
- Expanding the mind: insulin-like growth factor I and brain development.Endocrinology · 2008Review
- Article
- Remyelination in multiple sclerosis.International review of neurobiology · 2007Review
- Activation of proteasome by insulin-like growth factor-I may enhance clearance of oxidized proteins in the brain.Mechanisms of ageing and developmentArticle
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
In order to investigate a role for insulin-like growth factor-1 (IGF-1) in ameliorating the effects of demyelinating events and potentiating remyelination, we have generated transgenic (tg) mice expressing IGF-1 under the control of the myelin basic protein promoter. Heterozygous tg mice expressed the highest levels of IGF-1 in brain during the most active periods of myelination as determined by Western and Northern blotting. A high level of expression was found throughout the lives of the tg mice. There was no increased expression of IGF-1 in other organs. The brains of heterozygous mice were larger than those of normal mice by 2 weeks of age, and they continued to increase in size for several months. Light and electron microscopy showed extensive myelination of axons. Behavioral studies of the older heterozygous mice documented difficulty with balance. This new tg mouse model can be bred to mice that are heterozygous for genetic leukodystrophies to produce eventually mice that are affected with a given leukodystrophy but overexpress IGF-1 during myelination and remyelination. It will be interesting to see if overexpression of IGF-1 can modulate the pathological and clinical features of the inherited leukodystrophies with or without supplemental therapies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.