Category Ranking

98%

Total Visits

921

Avg Visit Duration

2 minutes

Citations

20

Article Abstract

Alzheimer's disease, a progressively degenerative neurological disorder, is the most common cause of dementia in the elderly. While its precise etiology remains unclear, researchers have identified diverse pathological characteristics and molecular pathways associated with its progression. Advances in scientific research have increasingly highlighted the crucial role of non-coding RNAs in the progression of Alzheimer's disease. These non-coding RNAs regulate several biological processes critical to the advancement of the disease, offering promising potential as therapeutic targets and diagnostic biomarkers. Therefore, this review aims to investigate the underlying mechanisms of Alzheimer's disease onset, with a particular focus on microRNAs, long non-coding RNAs, and circular RNAs associated with the disease. The review elucidates the potential pathogenic processes of Alzheimer's disease and provides a detailed description of the synthesis mechanisms of the three aforementioned non-coding RNAs. It comprehensively summarizes the various non-coding RNAs that have been identified to play key regulatory roles in Alzheimer's disease, as well as how these non-coding RNAs influence the disease's progression by regulating gene expression and protein functions. For example, miR-9 targets the UBE4B gene, promoting autophagy-mediated degradation of Tau protein, thereby reducing Tau accumulation and delaying Alzheimer's disease progression. Conversely, the long non-coding RNA BACE1-AS stabilizes BACE1 mRNA, promoting the generation of amyloid-β and accelerating Alzheimer's disease development. Additionally, circular RNAs play significant roles in regulating neuroinflammatory responses. By integrating insights from these regulatory mechanisms, there is potential to discover new therapeutic targets and potential biomarkers for early detection and management of Alzheimer's disease. This review aims to enhance the understanding of the relationship between Alzheimer's disease and non-coding RNAs, potentially paving the way for early detection and novel treatment strategies.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC12094571PMC
http://dx.doi.org/10.4103/NRR.NRR-D-24-00696DOI Listing

Publication Analysis

Top Keywords

alzheimer's disease
40
non-coding rnas
28
disease
12
alzheimer's
10
non-coding
9
rnas
9
non-coding rna
8
disease non-coding
8
therapeutic targets
8
review aims
8

Similar Publications

Background: Early identification of pathological α-synuclein deposition (αSynD) may improve understanding of Lewy body disorder (LBD) progression and enable timely disease-modifying treatments.

Objectives: We investigated αSynD using a seed amplification assay and assessed prodromal LBD symptoms in individuals with idiopathic olfactory dysfunction (iOD).

Methods: In this cross-sectional, case-control study, we included iOD participants and normosmic healthy controls (HC) aged 55 to 75 years without diagnoses of dementia with Lewy bodies, Parkinson's disease (PD), or other major neurological disorders.

View Article and Find Full Text PDF

Neurodegenerative disorders (NDD) i.e., dementia of the Alzheimer's type, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis are a rising worldwide epidemic driven by aging populations and characterized by progressive neuronal impairment.

View Article and Find Full Text PDF

Peripheral Inflammation Is Associated With Greater Neuronal Injury and Lower Episodic Memory Among Late Middle-Aged Adults.

J Neurochem

September 2025

Division of Neurogeriatrics, Center for Alzheimer Research, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden.

Elucidating the earliest biological mechanisms underlying Alzheimer's disease (AD) is critical for advancing early detection strategies. While amyloid-β (Aβ) and tau pathologies have been central to preclinical AD research, the roles of peripheral biological processes in disease initiation remain underexplored. We investigated patterns of F-MK6240 tau positron emission tomography (PET) and peripheral inflammation across stages defined by Aβ burden and neuronal injury in n = 132 (64.

View Article and Find Full Text PDF

Antibody Therapies for Alzheimer's Disease: A New Strategy for Targeted Therapy and Blood-Brain Barrier Delivery.

ACS Chem Neurosci

September 2025

Institute of Cell Engineering, School of Medicine, Johns Hopkins University, Baltimore, Maryland 21215, United States.

Alzheimer's disease (AD) is a neurodegenerative disease characterized by progressive cognitive impairment and neuronal loss, with pathological hallmarks including Aβ plaque deposition and tau tangles. At present, the early diagnosis and treatment of AD still face great challenges, such as limited diagnostic methods, difficulty in blood-brain barrier (BBB) penetration, complex disease mechanisms, and lack of highly effective targeted therapies. Antibody drugs have shown broad prospects in the field of AD due to their high specificity, engineering and multifunctional therapeutic potential, include targeted Aβ clearance, tau pathological regulation, imaging probes, and blood biomarkers.

View Article and Find Full Text PDF

Network Pharmacology of miR-146a-5p as a Potential Anti-Inflammatory Agent in Preventing Alzheimer's Disease.

Curr Alzheimer Res

September 2025

School of Biosciences, Faculty of Health and Medical Sciences, Taylor's University, 47500 Subang Jaya, Selangor, Malaysia.

Introduction: Alzheimer's disease is expressed as chronic neuroinflammation in the brain, which results in neuronal dysfunction, aberrant protein folding, and declining cognitive abilities. miR-146a-5p is a potent anti-inflammatory agent that can be used to treat several inflammatory diseases, as well as promote wound healing. Our research aimed to utilize network pharmacology to elucidate the therapeutic potential of miR-146a-5p in treating Alzheimer's disease using a biocomputational approach.

View Article and Find Full Text PDF