Evidence map›Paper›PMID 40982080›Full record

ReviewSaudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society2025

Non-coding RNA-mediated gene regulation in Alzheimer's disease pathogenesis: molecular insights and emerging innovations.

Sami I Alzarea

Abstract readReview
In one paragraph

Review in Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Review
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

1 author.

Sami I AlzareaDepartment of Pharmacology, College of Pharmacy, Jouf University, 72341, Sakaka, Al-Jouf, Saudi Arabia. samisz@ju.edu.sa.ORCID http://orcid.org/0000-0003-4007-4023

Funding

Al Jouf University DGSSR-2024-01-01074
6 · The paper itself

Abstract

The accumulation of pathological markers, such as tau tangles and amyloid-beta (Aβ) plaques, and progressive cognitive dysfunction are the markers of Alzheimer's disease (AD). The development of successful therapeutic plans requires exposure to the molecular mechanisms underlying AD development. The importance of non-coding RNAs (ncRNAs), such as circular RNAs (circRNAs), microRNAs (miRNAs), long ncRNAs (lncRNAs), and PIWI-interacting RNAs (piRNAs), in controlling gene expression and influencing the pathophysiology of disease has been brought to light by recent studies. With a focus on their role in important processes such tau hyperphosphorylation, neuroinflammation, and amyloid-beta formation, this study attempts to give a thorough overview of the several types of ncRNAs and their dysregulation in AD. The genetic variants that are associated with the function of ncRNA including single nucleotide polymorphisms (SNPs) may influence ncRNA expression and activity, thereby impacting the susceptibility of individual towards AD. Furthermore, the impact of biomarkers of ncRNAs for early diagnosis and therapeutic option for intervention, highlighting most recent advancement in high-throughput technologies and bioinformatics facilitating ncRNA profiling has also being discussed. The integration of multi-omics approaches and artificial intelligence, new advancement for the complex relationship among ncRNAs and AD pathology are also discussed. The enhancement and understanding of ncRNAs could lead to the door for novel therapeutic concepts for the mitigation of AD progression, offering effective interventions in a disease that currently starves the curative treatments.

Indexed as

Alzheimer's diseaseBiomarkersLong non-coding RNAsMicroRNAsNon-coding RNAs

Identifiers

PMID40982080
PMCPMC12454739

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.