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Role of MicroRNA-502-3p in Human Diseases
Davin Devara1, Yashmit Choudhary2, Subodh Kumar1,3
1Center of Emphasis in Neuroscience, Department of Molecular and Translational Medicine, Paul L. Foster School of Medicine, Texas Tech University Health Sciences Center, El Paso, TX 79905, USA.
Abstract:
MicroRNAs (miRNAs) are non-coding RNAs that play a major role in gene regulation in several diseases. MicroRNA-502-3p (MiR-502-3p) has been previously characterized in a variety of human diseases such as osteoporosis, diabetes, tuberculosis, cancers, and neurological disorders. Our studies recently explored the new role of miR-502-3p in regulating synapse function in Alzheimer's disease (AD). AD is the most common cause of dementia in elderly individuals. Synapse is the initial target that is hit during AD progression. The most common causes of synapse dysfunction in AD are amyloid beta, hyperphosphorylated tau, and microglia activation. MiR-502-3p was found to be localized and overexpressed in the AD synapses. Overexpression of miR-502-3p was correlated with AD severity in terms of Braak stages. Studies have shown that miR-502-3p modulates the glutaminergic and GABAergic synapse function in AD. The current study's emphasis is to discuss the in-depth roles of miR-502-3p in human diseases and AD and the future possibilities concerning miR-502-3p as a therapeutic for AD treatment.
Insights
MicroRNA-502-3p (miR-502-3p) is overexpressed in Alzheimer's disease (AD) synapses, impacting synapse function and disease severity. This microRNA shows potential as a therapeutic target for AD treatment.
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- MicroRNAs (miRNAs) are key regulators of gene expression implicated in various diseases.
- MicroRNA-502-3p (miR-502-3p) has been linked to osteoporosis, diabetes, tuberculosis, cancers, and neurological disorders.
- Synapse dysfunction, driven by amyloid beta, tau, and microglia, is an early event in Alzheimer's disease (AD).
Purpose of the Study:
- To explore the role of miR-502-3p in regulating synapse function in Alzheimer's disease (AD).
- To discuss the established roles of miR-502-3p in human diseases and AD.
- To examine the therapeutic potential of miR-502-3p for AD treatment.
Main Methods:
- Localization and expression analysis of miR-502-3p in AD synapses.
- Correlation analysis between miR-502-3p overexpression and AD severity (Braak stages).
- Investigation of miR-502-3p's modulation of glutamatergic and GABAergic synapse function in AD.
Main Results:
- MiR-502-3p was found to be localized and overexpressed within AD synapses.
- Higher levels of miR-502-3p correlated with increased AD severity.
- MiR-502-3p was shown to modulate both glutamatergic and GABAergic synapse functions in the context of AD.
Conclusions:
- MiR-502-3p plays a significant role in synapse dysfunction associated with Alzheimer's disease.
- The expression levels of miR-502-3p are linked to the progression and severity of AD.
- MiR-502-3p represents a promising therapeutic target for future Alzheimer's disease treatments.
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