Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2020 Jul 14;18(7):1037–1047. doi: 10.1080/15476286.2020.1788848

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 2020 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.

This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License (http://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited, and is not altered, transformed, or built upon in any way.

PMC Copyright notice

Figure 1. — Schematic of LncRNAs and their regulatory mechanisms in AD. LncRNAs modulate cellular process such as mRNA transcription (NDM29 and LRP1-AS), mRNA splicing (51A and GDNFOS), mRNA stability (Sox2OT, EBF3-AS, BDNF-AS, BACE1-AS and NAT-RAD18), and protein translation (LoNA and BC200). LncRNAs participate in AD pathology via having impact on Aβ metabolism (LRP1-AS, BACE-AS, 51A, NDM29 and NEAT1), tau hyperphosphorylation (NEAT1), neuroinflammation (NDM29, SNHG1 and MALAT1), synaptic plasticity (LoNA, BC200, GDNFOS and BDNF-AS), neurogenesis (Sox2OT), and neuronal cell death (EBF3-AS, NAT-Rad18, MALAT1, SNHG1, NEAT1 and BC200)