Evidence map›Paper›PMID 34621163›Full record

ArticleFrontiers in aging neuroscience2021

The Perspective of Dysregulated LncRNAs in Alzheimer's Disease: A Systematic Scoping Review.

Mohammad Reza Asadi, Mehdi Hassani, Shiva Kiani, Hani Sabaie, Marziyeh Sadat Moslehian, Mohammad Kazemi, Soudeh Ghafouri-Fard, Mohammad Taheri, Maryam Rezazadeh

Open access · goldAbstract readScoping Review
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in aging neuroscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 3 pooled it
2.4field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 3 syntheses or guidelines pooled it, 36 citations in OpenAlex.

  1. The Footprint ofCurrent Alzheimer research · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 5 institutions in 1 country.

Mohammad Reza AsadiMolecular Medicine Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Mehdi HassaniStudent Research Committee, University of Social Welfare and Rehabilitation Sciences, Tehran, Iran.
Shiva KianiDepartment of Molecular Genetics, School of Biological Sciences, Tarbiat Modares University, Tehran, Iran.
Hani SabaieStudent Research Committee, Tabriz University of Medical Sciences, Tabriz, Iran.
Marziyeh Sadat MoslehianDepartment of Medical Genetics, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
Mohammad KazemiDepartment of Social Medicine, Zanjan University of Medical Sciences, Zanjan, Iran.
Soudeh Ghafouri-FardDepartment of Medical Genetics, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Mohammad TaheriSkull Base Research Center, Loghman Hakim Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Maryam RezazadehMolecular Medicine Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Tabriz University of Medical Sciences · IRShahid Beheshti University of Medical Sciences · IRTarbiat Modares University · IRUniversity of Social Welfare and Rehabilitation Sciences · IRZanjan University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

LncRNAs act as part of non-coding RNAs at high levels of complex and stimulatory configurations in basic molecular mechanisms. Their extensive regulatory activity in the CNS continues on a small scale, from the functions of synapses to large-scale neurodevelopment and cognitive functions, aging, and can be seen in both health and disease situations. One of the vast consequences of the pathological role of dysregulated lncRNAs in the CNS due to their role in a network of regulatory pathways can be manifested in Alzheimer's as a neurodegenerative disease. The disease is characterized by two main hallmarks: amyloid plaques due to the accumulation of β-amyloid components and neurofibrillary tangles (NFT) resulting from the accumulation of phosphorylated tau. Numerous studies in humans, animal models, and various cell lines have revealed the role of lncRNAs in the pathogenesis of Alzheimer's disease. This scoping review was performed with a six-step strategy and based on the Prisma guideline by systematically searching the publications of seven databases. Out of 1,591 records, 69 articles were utterly aligned with the specified inclusion criteria and were summarized in the relevant table. Most of the studies were devoted to BACE1-AS, NEAT1, MALAT1, and SNHG1 lncRNAs, respectively, and about one-third of the studies investigated a unique lncRNA. About 56% of the studies reported up-regulation, and 7% reported down-regulation of lncRNAs expressions. Overall, this study was conducted to investigate the association between lncRNAs and Alzheimer's disease to make a reputable source for further studies and find more molecular therapeutic goals for this disease.

Indexed as

Alzheimer's diseaseBACE1-ASlncRNAsMALAT1NEAT1NFTSNHG1β-amyloid

Identifiers

PMID34621163
PMCPMC8490871
OpenAlexW3201297910

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.