Noncoding RNAs in Alzheimer's disease

Alzheimer's disease (AD) is a progressive neurodegenerative disorder and the main cause of dementia among the elderly worldwide. Despite intense efforts to develop drugs for preventing and treating AD, no effective therapies are available as yet, posing a growing burden at the personal, medical...

Full description

Saved in:
Bibliographic Details
Published in:Wiley interdisciplinary reviews. RNA Vol. 9; no. 2; pp. e1463 - n/a
Main Authors: Idda, M. Laura, Munk, Rachel, Abdelmohsen, Kotb, Gorospe, Myriam
Format: Journal Article
Language:English
Published: Hoboken, USA John Wiley & Sons, Inc 01.03.2018
Wiley Subscription Services, Inc
Subjects:
Alzheimer Disease - genetics
Alzheimer's disease
amyloid plaques
Amyloid precursor protein
Animals
circRNA
Dementia disorders
Drug development
Gene expression
Geriatrics
Humans
lncRNA
miRNA
neurodegeneration
Neurodegenerative diseases
Neurofibrillary tangles
noncoding RNA
Pathogenesis
Post-transcription
posttranscriptional gene regulation
RNA, Untranslated
Senile plaques
Tau protein
lncRNA
noncoding RNA
circRNA
neurofibrillary tangles
neurodegeneration
miRNA
posttranscriptional gene regulation
amyloid plaques
ISSN:1757-7004, 1757-7012, 1757-7012
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Alzheimer's disease (AD) is a progressive neurodegenerative disorder and the main cause of dementia among the elderly worldwide. Despite intense efforts to develop drugs for preventing and treating AD, no effective therapies are available as yet, posing a growing burden at the personal, medical, and socioeconomic levels. AD is characterized by the production and aggregation of amyloid β (Aβ) peptides derived from amyloid precursor protein (APP), the presence of hyperphosphorylated microtubule‐associated protein Tau (MAPT), and chronic inflammation leading to neuronal loss. Aβ accumulation and hyperphosphorylated Tau are responsible for the main histopathological features of AD, Aβ plaques, and neurofibrillary tangles (NFTs), respectively. However, the full spectrum of molecular factors that contribute to AD pathogenesis is not known. Noncoding (nc)RNAs, including microRNAs (miRNAs), long noncoding RNAs (lncRNAs), and circular RNAs (circRNAs), regulate gene expression at the transcriptional and posttranscriptional levels in various diseases, serving as biomarkers and potential therapeutic targets. There is rising recognition that ncRNAs have been implicated in both the onset and pathogenesis of AD. Here, we review the ncRNAs implicated posttranscriptionally in the main AD pathways and discuss the growing interest in targeting regulatory ncRNAs therapeutically to combat AD pathology. WIREs RNA 2018, 9:e1463. doi: 10.1002/wrna.1463 This article is categorized under: RNA in Disease and Development > RNA in Disease Schematic of the three main domains of AD pathogenesis. Top, APP is cleaved by α, β, and γ secretases; the generation and aggregation of amyloidogenic Aβ peptides outside of the cell leads to the formation of amyloid plaques. Bottom, the hyperphosphorylation of Tau protein results in formation of intracellular neurofibrillary tangles. Right, amyloid plaques and neurofibrillary tangles create a toxic environment characterized by neuroinflammation and neurodegeneration. Key, top right
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 14
ObjectType-Review-3
content type line 23
ISSN:1757-7004
1757-7012
1757-7012
DOI:10.1002/wrna.1463