ArticleMolecular therapy. Nucleic acids2022
The Aptamer Ob2, a novel AChE inhibitor, restores cognitive deficits and alleviates amyloidogenesis in 5×FAD transgenic mice.
Article in Molecular therapy. Nucleic acids, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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9 citing papers in PubMed, 17 citations in OpenAlex.
- Nucleic acid therapeutics in neurodegenerative disorders: emerging technologies and clinical landscape.Molecular neurodegeneration advances · 2026Review
- Zebrafish study provides evidence forFrontiers in cellular and infection microbiology · 2026Article
- Therapeutic Oligonucleotides for Neurodegenerative Diseases: Aptamer Strategies and Clay Nanoparticle-Based Delivery.Chemical record (New York, N.Y.) · 2025Review
- The Diagnostic and Therapeutic Potential of Oligonucleotide Aptamers in Alzheimer's Disease.Cells · 2025Review
- Mushroom-derived bioactive components with definite structures in alleviating the pathogenesis of Alzheimer's disease.Frontiers in pharmacology · 2024Review
- Exploring the Potential of Aptamers in Targeting Neuroinflammation and Neurodegenerative Disorders: Opportunities and Challenges.International journal of molecular sciences · 2023Review
- Anti-Neuroinflammatory Potential of Natural Products in the Treatment of Alzheimer's Disease.Molecules (Basel, Switzerland) · 2023Review
- A Novel Based-Network Strategy to Identify Phytochemicals from Radix Salviae Miltiorrhizae (Danshen) for Treating Alzheimer's Disease.Molecules (Basel, Switzerland) · 2022Article
- Effects ofFrontiers in pharmacology · 2022Article
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Authors and funding
11 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Loss of cerebral cholinergic neurons and decreased levels of acetylcholine (ACh) are considered to be major factors causing cognitive dysfunction in Alzheimer's disease (AD). Abnormally elevated levels of acetylcholinesterase (AChE) resulting in decreased levels of ACh are common in AD patients; thus, AChE inhibitors (AChEIs) are widely used for the treatment of AD. In our previous work, we acquired DNA aptamers Ob1, Ob2, and Ob3 against human brain AChE from systematic evolution of ligands by exponential enrichment (SELEX). In this study, we investigated the effect of these aptamers on learning and memory abilities, as well as the underlying mechanism in a 5×FAD transgenic AD mouse model. Here, we showed that only aptamer Ob2 exhibits a good inhibitory effect on both mouse and human AChE activity. In addition, chronic treatment with aptamer Ob2 significantly improved cognitive ability of 5×FAD mice in the Morris water maze. Moreover, the mechanism of aptamer Ob2 in 5×FAD mice may be associated with its inhibition of AChE activity, alleviation of the levels of Aβ by lowering the expression of β-secretase (BACE1), and activation of astrocytes in the brains of 5×FAD mice. These results indicate that aptamer Ob2 exhibits potential as an effective AChEI for the treatment of AD.
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