Serum insulin-like growth factor I in brain function
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- Carro Eva
- Cajal Institute, CSIC, Madrid
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- Torres-Aleman Ignacio
- Cajal Institute, CSIC, Madrid
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Abstract
Insulin-like growth factor I (IGF-I) is present at high concentrations in the circulation. Tissue-specific genetic ablation has shown that the majority of serum IGF-I is secreted by liver cells, although all major organs synthesize it. IGF-I is an important signal during development, including brain growth. Although the biological role of IGF-I in organs such as muscle or ovary is reasonably well established, its biological significance in the adult brain is far from clear. In this regard, while local IGF-I synthesis decreases during brain development, protein levels remain relatively constant throughout life until old age, where a decline is found, not only in the brain but also in the blood-stream. This mismatch between declining local synthesis early after birth and steady protein levels may be explained by the ability of serum IGF-I to access the brain across the blood-brain-barrier. This peripheral IGF-I input to the brain is a physiologically meaningful process of potential impact in brain diseases. Numerous brain mechanisms are regulated by serum IGF-I. Many of these, such as cell energy modulation or growth and survival are common to other IGF-I target tissues but there are also a number of brain-specific mechanisms regulated by IGF-I which likely underlie the ability of serum IGF-I to modulate the major function of the brain: cognition. We propose that serum IGF-I forms part of the mechanisms involved in the “cognitive reserve” concept of brain responses to homeostasis breakdown. Based on IGF-I pleiotropy not only in brain but elsewhere, we consider that loss of IGF-I function is an important step towards disease.
Journal
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- The Keio Journal of Medicine
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The Keio Journal of Medicine 55 (2), 59-63, 2006
The Keio Journal of Medicine
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Details 詳細情報について
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- CRID
- 1390282681314430208
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- NII Article ID
- 10018350544
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- NII Book ID
- AA00710216
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- COI
- 1:CAS:528:DC%2BD28Xot1Cnsb4%3D
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- ISSN
- 18801293
- 00229717
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- PubMed
- 16830417
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- Text Lang
- en
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- Data Source
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- JaLC
- Crossref
- PubMed
- CiNii Articles
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- Abstract License Flag
- Disallowed