Abstract
Non-syndromic intellectual disability (NS-ID or idiopathic) is a complex neurodevelopmental disorder that represents a global health issue. Although many efforts have been made to characterize it and distinguish it from syndromic intellectual disability (S-ID), the highly heterogeneous aspect of this disorder makes it difficult to understand its etiology. Long noncoding RNAs (lncRNAs) comprise a large group of transcripts that can act through various mechanisms and be involved in important neurodevelopmental processes. In this sense, comprehending the roles they play in this intricate context is a valuable way of getting new insights about how NS-ID can arise and develop. In this review, we attempt to bring together knowledge available in the literature about lncRNAs involved with molecular and cellular pathways already described in intellectual disability and neural function, to better understand their relevance in NS-ID and the regulatory complexity of this disorder.
Highlights
Intellectual disability (ID) is characterized by significant intellectual functioning limitation and adaptive behavior occurring before the age of 18 [1]
Many of them have been described as human embryonic stem cells pluripotency regulators, like lncPRESS1, that controls a gene network that controls pluripotency [13], and GAS5, a Long noncoding RNAs (lncRNAs) that is directly regulated by pluripotency factors and acts on hESCs self-renewal [14]
Some lncRNAs have already been associated with neural development, such as PNKY, a transcript involved in the suppression of neuronal commitment of neural stem cells (NSCs) [17], FMR4, a lncRNA that promotes the proliferation of human neural precursor cells (NPCs) [18], and splicing variants of the lncRNA C130071C03Riken, which are involved in neural differentiation [19]
Summary
Intellectual disability (ID) is characterized by significant intellectual functioning limitation and adaptive behavior occurring before the age of 18 [1] It is usually defined by an intelligence quotient (IQ) of less than 70 and severe deficiency in the environment and social milieu adaptation [2], which can be caused by genetic, prenatal, and environmental factors, representing a health issue in both developed and developing countries [3]. More than 200 candidate genes have been associated with NS-ID, most of which are not shared between NS-ID and S-ID and/or neurological and neuropsychiatric diseases [10] Taken all together, these show the efforts being made to understand the etiology of NS-ID and demonstrate the complexity of trying to define this heterogeneous disorder
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