MicroRNAs in Extracellular Vesicles of Alzheimer’s Disease
Open accessAbstract
Alzheimer’s disease (AD) is a neurodegenerative disease with dysfunction of memory, language and thinking. More than 55 million people were diagnosed with AD or other dementia around the world in 2020. The pathology of AD is still unclear and there are no applicable therapies for AD. MicroRNAs (miRNAs) play key roles in AD pathology and have great potential for the diagnosis and treatment of AD. Extracellular vesicles (EVs) widely exist in body fluids such as blood and cerebrospinal fluid (CSF) and contain miRNAs that are involved in cell-to-cell communication. We summarized the dysregulated miRNAs in EVs derived from the different body fluids of AD patients, as well as their potential function and application in AD. We also compared these dysregulated miRNAs in EVs to those in the brain tissues of AD patients aiming to provide a comprehensive view of miRNAs in AD. After careful comparisons, we found that miR-125b-5p and miR-132-3p were upregulated and downregulated in several different brain tissues of AD and EVs of AD, respectively, suggesting their value in AD diagnosis based on EV miRNAs. Furthermore, miR-9-5p was dysregulated in EVs and different brain tissues of AD patients and had also been tested as a potential therapy for AD in mice and human cell models, suggesting that miR-9-5p could be used to design new therapies for AD.
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ABCA1‐Labeled Exosomes in Serum Contain Higher MicroRNA‐193b Levels in Alzheimer’s Disease
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MiR-9-5p inhibits mitochondrial damage and oxidative stress in AD cell models by targeting GSK-3β
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MicroRNA-135a in ABCA1-labeled Exosome is a Serum Biomarker Candidate for Alzheimer's Disease.
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In Vitro Amyloid Aggregate Forming Ability of TGFBI Mutants that Cause Corneal Dystrophies
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KLF12 transcriptional activation by a novel LncRNA A930015D03Rik enhances melanoma metastasis
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MicroRNA cargo in neuron‐derived vesicles as peripheral biomarkers of brain insulin dysregulation
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- Authors
- Li, W., & Zheng, Y.
- Affiliations
- Kunming University of Science and Technology (CN)
- Yunnan Agricultural University (CN)
- Corresponding author
- Zheng, Yun
- ORCID
- Zheng, Yun
- Venue
- Cells
- Publisher
- MDPI AG
- Published
- 2023-05-13
- Volume
- 12
- Issue
- 10
- Pages
- 1378
- ISSN
- 2073-4409 (ISSN-L)
- PMC
- PMC10216432
- OpenAlex
- W4382813296
- Semantic Scholar
- bdbf284804ad9a0d37ec765475b591d1e86e01db
- Cited by
- 43
- References
- 110
- Citations by year
- 2026: 17 · 2025: 12 · 2024: 11 · 2023: 2
- FWCI
- 1.06
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Cells (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Natural Science Foundation of China (31460295, SKLGE-2107)
- State Key Laboratory of Genetic Engineering, Fudan University, China (31460295, SKLGE-2107)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Extracellular vesicles in disease
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Keywords
- Alzheimer's disease, microRNA, extracellular vesicles, miR-125b-5p, miR-132-3p, miR-9-5p, cerebrospinal fluid, biomarkers, diagnosis, therapeutic target, microRNA dysregulation, brain tissue
- MeSH terms
- Extracellular Vesicles, Alzheimer Disease, Animals, Humans, Neurodegenerative Diseases, MicroRNAs, Mice
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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