ArticleAmerican journal of neurodegenerative disease2014
Identification of microRNAs involved in Alzheimer's progression using a rabbit model of the disease.
Article in American journal of neurodegenerative disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
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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.
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Who cites it
31 citing papers in PubMed, 43 citations in OpenAlex.
- STZ‑induced sporadic Alzheimer's in rats: behavioral, histopathological, and MiRNA profiles.Journal of molecular histology · 2026Article
- Let-7 Family as a Mediator of Exercise on Alzheimer's Disease.Cellular and molecular neurobiology · 2025Review
- A review on gut microbiota and miRNA crosstalk: implications for Alzheimer's disease.GeroScience · 2025Review
- miRNA and leptin signaling in metabolic diseases and at extreme environments.Pharmacology research & perspectives · 2024Review
- Mesenchymal Stem Cells from Familial Alzheimer's Patients Express MicroRNA Differently.International journal of molecular sciences · 2024Article
- Emerging Role of MicroRNA-30c in Neurological Disorders.International journal of molecular sciences · 2022Review
- Lipopolysaccharides (LPSs) as Potent Neurotoxic Glycolipids in Alzheimer's Disease (AD).International journal of molecular sciences · 2022Review
- Let-7 as a Promising Target in Aging and Aging-Related Diseases: A Promise or a Pledge.Biomolecules · 2022Review
- Downregulation of Neurofilament Light Chain Expression in Human Neuronal-Glial Cell Co-Cultures by a Microbiome-Derived Lipopolysaccharide-Induced miRNA-30b-5p.Frontiers in neurology · 2022Article
- Identifying Key MicroRNA Signatures for Neurodegenerative Diseases With Machine Learning Methods.Frontiers in genetics · 2022Article
- MiR-9-5p Inhibits the MMPOxidative medicine and cellular longevity · 2022Article
- Inflammation, Nitro-Oxidative Stress, Impaired Autophagy, and Insulin Resistance as a Mechanistic Convergence Between Arterial Stiffness and Alzheimer's Disease.Frontiers in molecular biosciences · 2021Review
- Insulin resistance: a connecting link between Alzheimer's disease and metabolic disorder.Metabolic brain disease · 2021Review
- GuanXinNing Tablet Attenuates Alzheimer's Disease via Improving Gut Microbiota, Host Metabolites, and Neuronal Apoptosis in Rabbits.Evidence-based complementary and alternative medicine : eCAM · 2021Article
- Semaphorin 3A Contributes to Secondary Blood-Brain Barrier Damage After Traumatic Brain Injury.Frontiers in cellular neuroscience · 2019Article
- MicroRNA-98 reduces amyloid β-protein production and improves oxidative stress and mitochondrial dysfunction through the Notch signaling pathway via HEY2 in Alzheimer's disease mice.International journal of molecular medicine · 2019Article
- A workflow for the integrative transcriptomic description of molecular pathology and the suggestion of normalizing compounds, exemplified by Parkinson's disease.Scientific reports · 2018Article
- Review
- miR-26b inhibits total neurite outgrowth, promotes cells apoptosis and downregulates neprilysin in Alzheimer's disease.International journal of clinical and experimental pathology · 2018Article
- MicroRNA expression patterns in human anterior cingulate and motor cortex: A study of dementia with Lewy bodies cases and controls.Brain research · 2018Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Alzheimer's disease (AD) is the most common neurodegenerative disorder characterized by the presence of extracellular plaques of β-amyloid peptides and intracellular tangles of hyperphosphorylated tau proteins in the brain. The vast majority of cases are late onset AD (LOAD), which are genetically heterogeneous and occur sporadically. High blood cholesterol is suggested to be a risk factor for this disease. Several neuropathological changes of LOAD can be reproduced by supplementing a rabbit's diet with 2% cholesterol for 12 weeks. Accumulating data in the literature suggest that microRNAs (miRNA) participate in the development of AD pathology. The present study focuses on the survey of changes of miRNA expression in rabbit brains during the progression of AD-like pathology using microarray followed by Taq-Man qRT-PCR analyses. Out of 1769 miRNA probes used in the experiments, 99 miRNAs were found to be present in rabbit brain, 57 were newly identified as miRNAs from rabbit brain. Eleven miRNAs showed significant changes over AD-like pathology progression. Among them, the changes of miR-125b, miR-98, miR-107, miR-30, along with 3 members of the let-7 family were similar to those observed in human AD samples, whereas the expression patterns of miR-15a, miR-26b, miR-9 and miR-576-3p were unique to this rabbit LOAD model. The significant up regulation of miR-26b is consistent with the decrease of leptin levels in the brains of cholesterol fed rabbit model for AD, confirming that miR-26b is indeed regulated by leptin and that both leptin and miR-26b may be involved in cholesterol induced AD-like pathology.
Indexed as
Identifiers
24754001PMC3986609W36436465What 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.