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Neurodegenerative disease

Cones go hungry

Nature Reviews Neuroscience volume 10, pages 84–85 (2009)Cite this article

The authors examined four different strains of mice that carry mutations associated with RP to investigate the molecular events that are taking place when cones begin to die. Microarray analysis revealed a common pattern of transcript expression: of 230 genes that were specifically upregulated at the onset of cone death in all 4 strains, a large proportion was associated with cellular metabolism, including 12 that were associated with the insulin–mammalian target of rapamycin (mTOR; also known as FRAP1) signalling pathway.

mTOR signalling is involved in regulating cellular metabolism in response to changes in cellular energy levels. Levels of phosphorylated (active) mTOR were found to decrease in cones during the period of cone degeneration, suggesting that there is a decrease in glucose levels in these cells. Furthermore, the authors also observed an upregulation of hypoxia inducible factor 1α (HIF1α) — a transcription factor that responds to changes in mTOR activity — and of one of its targets, glucose transporter 1 (GLUT1; also known as SLC2A1), in these cells. They showed that chaperone-mediated autophagy, a typical response to prolonged lack of nutrients, occurred in the dying cones.

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ORIGINAL RESEARCH PAPER

  1. Punzo, C., Kornacker, K. & Cepko, C. L. Stimulation of the insulin/mTOR pathway delays cone death in a mouse model of retinitis pigmentosa. Nature Neurosci. 7 Dec 2008 (doi: 10.1038/nn.2234)

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  1. Katherine Whalley
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Whalley, K. Cones go hungry. Nat Rev Neurosci 10, 84–85 (2009). https://doi.org/10.1038/nrn2574

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