ReviewLong non-coding RNAs in brain development, synaptic biology, and Alzheimer's disease

- LncRNAs emerge as regulators in brain development and synaptic physiology.
- Aberrant lncRNAs were found in the pathologic process of AD.
- LncRNAs cause abnormal Aβ peptide accumulation and synaptic failure.
- LncRNAs play a role in gene regulations in neurotrophin depletion and inflammation.
- LncRNAs are implicated in mitochondrial dysfunction and stress response.

Long non-coding RNAs (lncRNAs), which are long transcripts without apparent protein-coding roles, interfere with gene expression and signaling events at various stages. Increasing evidence has suggested that lncRNAs function in the regulation of tissue homeostasis and under pathophysiologic conditions. In the nervous system, the expression of lncRNAs has been detected and characterized under normal physiologic conditions and in disease states. Some lncRNAs regulate brain development and synaptic plasticity. In Alzheimer's disease (AD), several lncRNAs have been demonstrated to regulate β-amyloid production/generation, synaptic impairment, neurotrophin depletion, inflammation, mitochondrial dysfunction, and stress responses. This review summarizes data on lncRNA expression and focuses on neural lncRNAs that may function in AD. Although our understanding of lncRNAs remains in its infancy, this review provides insight into the contribution of lncRNAs to AD.