Table 1.

The lncRNAs implicated in the etiology of ID.

lncRNAs Directly Involved in ID
lncRNA	Observed Anomaly	Associated Phenotype Observed		Mechanism/Evidence
lnc-NR2F1	[t(5:12)]	Developmental and speech delay		Disruption of lnc-NR2F1, which controls neuronal migration and other NDD-genes
LINC00299	2p25.1 disruption	Speech delay, ID, bipolar disorder, epilepsy, Angelman-like syndrome		LINC00299 increased levels in patients
lncRNAs regulating genes involved in ID
lncRNA	Regulated gene	Possible association with disease	OMIM disease	Mechanism/Evidence
BC200	FMR1	Fragile-X syndrome	#300624	Repression of local translation, interacting with FMRP
GAS5	GSTM3	Down syndrome	#190685	Downregulation of GAS5 in DS patients Upregulation in Klinefelter syndrome patients
NRON	NFAT	Down syndrome	#190685	Reduced NFAT causes DS-like phenotype; NRON modulates NFAT activity.
EVF2	MECP2	Rett syndrome X-linked intellectual developmental disorder	#312750 #300055 #300260	EVF2 associates with MECP2 at regulatory elements in interneurons, controlling DLX5, DLX6 and GAD1 expression
AK081227 AK087060	MECP2	Rett syndrome X-linked intellectual developmental disorder	#312750 #300055 #300260	Upregulated levels in Mecp2-null mice; AK081227 downregulates Gabrr2
ZEB2-NAT	ZEB2	Mowat–Wilson syndrome	#235730	ZEB2-NAT controls ZEB2 by retaining the first intron of ZEB2 pre-mRNA
RMST	SOX2	Microphthalmia and optic nerve hypoplasia and abnormalities of the central nervous system	#206900	RMST physically associates with SOX2 regulating neurogenesis pathways
Sox2ot	SOX2	Microphthalmia and optic nerve hypoplasia and abnormalities of the central nervous system	#206900	Sox2ot represses SOX2 RNA levels
SYNGAP1-AS	SYNGAP1	Mental Retardation Autosomal Dominant 5	#612621	SYNGAP1-AS is upregulated in post-mortem brains