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miR-101a-3p Impairs Synaptic Plasticity and Contributes to Synucleinopathy.
Mary Xylaki1, Isabel Paiva1,2, Mohammed Al-Azzani1
1Department of Experimental Neurodegeneration, Centre for Biostructural Imaging of Neurodegeneration, University Medical Centre Göttingen, Göttingen, Germany.
Journal of Parkinson'S Disease
|February 6, 2023
Summary
This study reveals that elevated levels of microRNA-101a-3p are linked to alpha-synuclein pathology in synucleinopathies. This microRNA plays a dynamic role in synaptic plasticity, impacting neuronal function.
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- Synucleinopathies involve abnormal alpha-synuclein (aSyn) aggregation, leading to synaptic dysfunction and transcript deregulation.
- Synaptic compromise is a hallmark of synucleinopathies, correlating with aSyn accumulation.
Purpose of the Study:
- To identify microRNAs (miRNAs) involved in synaptic processes relevant to synucleinopathies.
- To investigate the role of specific miRNAs in synaptic dysfunction and degeneration.
Main Methods:
- Small RNA sequencing in transgenic mice expressing mutant aSyn (A30P).
- Validation using real-time quantitative polymerase chain reaction (qPCR).
- Functional analysis in primary neurons via biochemical assays and imaging.
Main Results:
- Upregulation of miR-101a-3p in aSyn transgenic mice and dementia with Lewy bodies patients.
- Overexpression of miR-101a-3p led to downregulation of postsynaptic proteins (GABA Ab2, SAPAP3) and altered dendritic morphology.
- Recombinant wild-type aSyn increased miR-101a-3p levels in neurons; enriched environment downregulated miR-101a-3p, indicating a dynamic role in plasticity.
Conclusions:
- Pathologic alpha-synuclein correlates with increased miR-101a-3p levels.
- miR-101a-3p has a novel, dynamic role in regulating synaptic plasticity.
- Findings suggest miR-101a-3p as a potential therapeutic target for synucleinopathies.
