Intriguingly, the genes dysregulated in HD human brain samples overlap with pathways affected by a reduction in NEAT1, confirming the correlation of NEAT1L and HD-induced perturbations.
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.
Previously described lncRNAs TUG1 (necessary for retinal development) and NEAT1 (a structural component of nuclear paraspeckles) are upregulated in HD caudate, while the brain-specific tumour-suppressor MEG3 is downregulated.