ReviewMolecular neurobiology2025
Long Non-Coding RNAs: Crucial Regulators in Alzheimer's Disease Pathogenesis and Prospects for Precision Medicine.
Review in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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.
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.
Who cites it
3 citing papers in PubMed.
- Lead Induces Mitochondrial Dysregulation in SH-SY5Y Neuroblastoma Cells via a lncRNA/circRNA-miRNA-mRNA Interdependent Networks.International journal of molecular sciences · 2025Article
- Cannabinerol Restores mRNA Splicing Defects Induced by β-Amyloid in an In Vitro Model of Alzheimer's Disease: A Transcriptomic Study.International journal of molecular sciences · 2025Article
- Direct and indirect role of non-coding RNAs in company with amyloid and tau protein in promoting neuroinflammation in post-ischemic brain neurodegeneration.Frontiers in cellular neuroscience · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
Long non-coding RNAs (LncRNAs) have emerged as pivotal regulators in the pathogenesis of Alzheimer's disease (AD), a progressive neurodegenerative disorder characterized by cognitive decline and memory loss. With the capacity to modulate gene expression at various levels, LncRNAs are implicated in multiple pathological mechanisms of AD, including amyloid-beta (Aβ) accumulation, tau protein phosphorylation, neuroinflammation, and neuronal apoptosis. Recent studies have highlighted the potential of LncRNAs as diagnostic biomarkers and therapeutic targets due to their differential expression patterns in AD patients. This review synthesizes current knowledge on the role of LncRNAs in AD, focusing on their involvement in key molecular pathways and their promise as indicators for early diagnosis and prognosis. We discuss the regulatory networks of LncRNAs in the context of AD, their interaction with miRNAs, and the implications for developing novel therapeutic strategies. Despite the complexity and variability in LncRNA function, the prospect of harnessing these molecules for precision medicine in AD is gaining momentum. The translational potential of LncRNA-based interventions offers a new frontier in the quest for effective treatments and a deeper understanding of the molecular underpinnings of AD.
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Identifiers
39907902What OpenQuestion holds
Registered trials
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.