Implications of Long Non-Coding RNAs in Age-Altered Proteostasis
Catana Cristina-Sorina, Crișan Catalina-Angela, Opre Dana, Berindan-Neagoe Ioana
Table 2 Senescence- associated lncRNAs and neurodegenerative disorders.
lncRNA/expressionImplication in neurodegenerative disordersAbnormalities in neuronal process/ Clinical featuresReference
MEG3
-expressed in the nucleus and cytoplasm
-upregulated in the hippocampus of old mice;
-downregulated in old induced striatal medium-sized spiny neurons (MSSNs); - PTEN/PI3K/AKT signaling cascade
-cognitive decline
-downregulated in HD brain tissue - synaptic plasticity in neurons
[30], [92]
SORL1-AS- upregulated in AD disease brain affecting Aβ formation-AD;
-Protein aggregation; -cognitive impairment
[30], [93]
Six3OS
-spatiotemporal expression
- Regulation of Six3 targets through interactions with Eya proteins and the chromatin-modifying protein Ezh2;- adult mouse neurogenesis[94]
17A-upregulated in frontal and temporal cortices
-increases Aβ secretion
-AD;
-Abolish GABA B2 intracellular signaling
[95]
MALAT-1- upregulated in human aged SVZ;
-upregulated in the hippocampus of old mice; - scaffold for proteins and RNAs
-cognitive decline;
-neurodegeneration; -PD
[30], [96], [97]
UCHL1-AS-downregulated in murine dopaminergic cells;
- regulated by a transcription factor Nurr1 required for dopamine cells differentiation
- Neurodegeneration;
-PD
[50]
ANRIL-altered expression in all tissues-AD;
- Neurodegeneration;
[98]
HOTAIR- high expression of HOTAIR promotes PD-PD[99]
BACE1-AS- Increases BACE1 mRNA stability and Aβ42 formation- up-regulated in AD brains[100], [101]