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Insulin-Like Growth Factor-1 and Neuroinflammation. | LitMetric

Insulin-Like Growth Factor-1 and Neuroinflammation.

Front Aging Neurosci

Laboratory of Neuroanatomy and Experimental Neurology, Department of Morphological Sciences, CIMUS, University of Santiago de Compostela, Santiago de Compostela, Spain.

Published: November 2017

AI Article Synopsis

  • - IGF-1's role in aging and neurodegeneration is debated, but it is known to influence neuroinflammation, with some studies showing it can both inhibit and promote inflammation depending on the context.
  • - In the brain, IGF-1 appears to protect neurons and reduce inflammation by affecting astrocytes and microglia, though its effectiveness may decrease with age, leading to a more pro-inflammatory state.
  • - The relationship between IGF-1, estrogen, and the renin-angiotensin system suggests that IGF-1 levels are important for managing neuroinflammation, particularly by promoting a protective M2 microglial phenotype, which becomes less effective as one ages.

Article Abstract

Insulin-like growth factor-1 (IGF-1) effects on aging and neurodegeneration is still controversial. However, it is widely admitted that IGF-1 is involved in the neuroinflammatory response. In peripheral tissues, several studies showed that IGF-1 inhibited the expression of inflammatory markers, although other studies concluded that IGF-1 has proinflammatory functions. Furthermore, proinflammatory cytokines such as TNF-α impaired IGF-1 signaling. In the brain, there are controversial results on effects of IGF-1 in neuroinflammation. In addition to direct protective effects on neurons, several studies revealed anti-inflammatory effects of IGF-1 acting on astrocytes and microglia, and that IGF-1 may also inhibit blood brain barrier permeability. Altogether suggests that the aging-related decrease in IGF-1 levels may contribute to the aging-related pro-inflammatory state. IGF-1 inhibits the astrocytic response to inflammatory stimuli, and modulates microglial phenotype (IGF-1 promotes the microglial M2 and inhibits of M1 phenotype). Furthermore, IGF-1 is mitogenic for microglia. IGF-1 and estrogen interact to modulate the neuroinflammatory response and microglial and astrocytic phenotypes. Brain renin-angiotensin and IGF-1 systems also interact to modulate neuroinflammation. Induction of microglial IGF-1 by angiotensin, and possibly by other pro-inflammatory inducers, plays a major role in the repression of the M1 microglial neurotoxic phenotype and the enhancement of the transition to an M2 microglial repair/regenerative phenotype. This mechanism is impaired in aged brains. Aging-related decrease in IGF-1 may contribute to the loss of capacity of microglia to undergo M2 activation. Fine tuning of IGF-1 levels may be critical for regulating the neuroinflammatory response, and IGF-1 may be involved in inflammation in a context-dependent mode.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5675852PMC
http://dx.doi.org/10.3389/fnagi.2017.00365DOI Listing

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