ArticleMolecular medicine reports2014
Attenuated ability of BACE1 to cleave the amyloid precursor protein via silencing long noncoding RNA BACE1‑AS expression.
Article in Molecular medicine reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.
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Who cites it
67 citing papers in PubMed, 1 synthesis or guideline pooled it, 108 citations in OpenAlex.
- Long Non-coding RNA: Insight Into Mechanisms of Alzheimer's Disease.Frontiers in molecular neuroscience · 2021Pooled it
- lncRNAs: key player in Aβ deposition.RNA biology · 2026Review
- miR-584-5p suppresses AβActa neurologica Belgica · 2026Article
- Long non-coding RNAs in neurodegenerative diseases - Molecular mechanisms, liquid biopsy biomarkers, and therapeutic targets: A review.Biomolecules & biomedicine · 2026Review
- Role of ncRNAs in Neurological Disorders and Cardiovascular Diseases.Experientia supplementum (2012) · 2026Review
- A systematic review on type 3 diabetes: bridging the gap between metabolic dysfunction and Alzheimer's disease.Diabetology & metabolic syndrome · 2025Review
- Untangling the Genetic Threads of Alzheimer's: Insights into Risk Factors and Biomarkers.Current gene therapy · 2025Review
- Is the Relationship Between Cardiovascular Disease and Alzheimer's Disease Genetic? A Scoping Review.Genes · 2024Article
- Identification, genomic localization, and functional validation of salt-stress-related lncRNAs in Indian Mustard (Brassica juncea L.).BMC genomics · 2024Article
- Distinct Hippocampal Expression Profiles of lncRNAs in Obese Type 2 Diabetes Mice Exhibiting Cognitive Impairment.Neuromolecular medicine · 2024Article
- In vivo and ex vivo gene therapy for neurodegenerative diseases: a promise for disease modification.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- Exploring the Frontier: Antisense Long Non-Coding RNAs as Key Regulators in Alzheimer's Disease.Aging and disease · 2024Review
- Article
- Alzheimer's Disease-Related Epigenetic Changes: Novel Therapeutic Targets.Molecular neurobiology · 2024Review
- The Role of Non-coding RNAs in Alzheimer's Disease: Pathogenesis, Novel Biomarkers, and Potential Therapeutic Targets.CNS & neurological disorders drug targets · 2024Review
- The Emerging Role of Autophagy-Associated lncRNAs in the Pathogenesis of Neurodegenerative Diseases.International journal of molecular sciences · 2023Review
- The Role of miR-128 in Neurodegenerative Diseases.International journal of molecular sciences · 2023Review
- Identification and characterization of noncoding RNAs-associated competing endogenous RNA networks in major depressive disorder.World journal of psychiatry · 2023Article
- Role of non‑coding RNAs as biomarkers and the application of omics technologies in Alzheimer's disease (Review).International journal of molecular medicine · 2023Review
- Review
7 more citing papers are in PubMed but not listed here.
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7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although large numbers of long noncoding RNAs (lncRNAs) expressed in the mammalian nervous system have been detected, their functions and mechanisms of regulation remain to be fully clarified. It has been reported that the lncRNA antisense transcript for β‑secretase‑1 (BACE1‑AS) is elevated in Alzheimer's disease (AD) and drives the rapid feed‑forward regulation of β‑secretase, suggesting that it is critical in AD development. In the present study, the senile plaque (SP) AD SH‑SY5Y cell model was established using the synthetic amyloid β‑protein (Aβ) 1‑42 in vitro. Using this model, the potential of siRNA‑mediated silencing of lncRNA BACE1‑AS expression to attenuate the ability of β‑secretase‑1 (BACE1) to cleave amyloid precursor protein (APP) and to reduce the production of Aβ1‑42 oligomers was investigated. MTT assays demonstrated that exogenous Aβ1‑42 suppressed SH‑SY5Y cell proliferation and induced APP‑related factor expression and SP formation. Furthermore, quantitative polymerase chain reaction and western blot analysis revealed that the mRNA and protein expression of Aβ1‑42 and Aβ1‑40 was significantly increased in the AD model group, with a marked decrease in Ki‑67 expression at day six. RNase protection assays (RPA) and northern blotting analysis confirmed that exogenous Aβ1‑42 not only promoted the expression of the APP‑cleaving enzyme BACE1, but also induced lncRNA BACE1‑AS expression. Furthermore, lncRNA BACE1‑AS formed RNA duplexes and increased the stability of BACE1 mRNA. Downregulation of lncRNA BACE1‑AS expression in SH‑SY5Y cells by siRNA silencing resulted in the attenuation of the ability of BACE1 to cleave APP and delayed the induction of SP formation in the SP AD SH‑SY5Y cell model.
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