NEAT1 (Nuclear Enriched Abundant Transcript 1), a long non-coding RNA molecule, might be protecting neurons in Huntington’s disease (HD), a new study suggests.
“Our observations support the notion that NEAT1 upregulation in HD contributes to the neuroprotective mechanism against neuronal injury rather than the pathological process underlying neurodegeneration in HD,” according to authors of the study “Altered Expression of the Long Noncoding RNA NEAT1 in Huntington’s Disease,” published recently in Molecular Neurobiology.
Research results could help identify potential targets for developing long non-coding RNA based approaches to treat HD.
The team led by Manho Kim, used microarray analysis to evaluate changes in the expression profile of long non-coding RNAs in HD. They focused particularly on NEAT1 observing that levels of this protein were increased in the brain of a mouse model of HD as well as in post-mortem brain samples of HD patients.
To understand the effect of NEAT1 on the survival of nerve cells, researchers transfected (forcibly introduced) mouse nerve cells grown in the laboratory with NEAT1. When they injured the cells, they saw that those transfected with NEAT1 survived better than those that were not.
Researchers concluded that NEAT1 over expression seen in HD might actually play a role in protecting nerve cells from dying rather than being part of the pathological process observed in HD.
NEAT1 is a novel long non-coding RNA found in the nucleus of cells. Long-non coding RNAs are molecules that are not able to code for a protein but that are involved in many biological processes such as regulation of gene expression and cellular differentiation. Understanding the exact involvement of NEAT1 in HD may help develop new therapeutic strategies in the future.
A collaboration between researchers at the University of Leicester, U.K., and the University of Maryland School of Medicine, Baltimore, may lead to a way of reversing some symptoms of neurogedenerative diseases, like Huntington’s, by blocking two specific enzymes of the kynurenine pathway.
The findings, published in the Proceedings of the National Academy of Sciences of the USA, are included in the study “Tryptophan-2,3-dioxygenase (TDO) inhibition ameliorates neurodegeneration by modulation of kynurenine pathway metabolites.”
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