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Related Experiment Video

Updated: Jan 27, 2026

Generation of Alpha-Synuclein Preformed Fibrils from Monomers and Use In Vivo

Generation of Alpha-Synuclein Preformed Fibrils from Monomers and Use In Vivo

Published on: June 2, 2019

Alpha-synuclein targets GluN2A NMDA receptor subunit causing striatal synaptic dysfunction and visuospatial memory

Valentina Durante¹, Antonio de Iure^1,2, Vittorio Loffredo^3,4

¹Neurological Clinic, Department of Medicine, Hospital Santa Maria della Misericordia, University of Perugia, Perugia, Italy.

Brain : a Journal of Neurology

|March 31, 2019

Summary

This summary is machine-generated.

Alpha-synuclein oligomers impair synaptic function in Parkinson's disease by reducing N-methyl-d-aspartate (NMDA) receptor activity. Targeting alpha-synuclein with antibodies may counteract these synaptic deficits.

Keywords:

Parkinson’s disease dopamine glutamate long-term potentiation monoclonal antibodies

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Published on: October 26, 2010

Area of Science:

Neuroscience
Molecular Biology
Pathology

Background:

Parkinson's disease (PD) involves altered dopaminergic signaling and the pathological aggregation of alpha-synuclein.
Alpha-synuclein oligomers are implicated in synaptic dysfunction, contributing to motor and cognitive deficits in PD.

Purpose of the Study:

To investigate the direct impact of alpha-synuclein on synaptic transmission and plasticity in Parkinson's disease models.
To identify the specific molecular targets of alpha-synuclein in synaptic dysfunction.

Main Methods:

Electrophysiology, optogenetics, immunofluorescence, molecular biology, and behavioral analyses were employed.
Studies were conducted on striatal slices and in vivo models of Parkinson's disease.

Main Results:

Alpha-synuclein reduces N-methyl-d-aspartate (NMDA) receptor-mediated currents and impairs corticostriatal long-term potentiation.
Intrastriatal alpha-synuclein injections caused visuospatial learning deficits linked to reduced GluN2A NMDA receptor subunit function.
Antibodies targeting alpha-synuclein prevented synaptic plasticity loss and GluN2A subunit reduction.

Conclusions:

Alpha-synuclein directly impairs synaptic function by targeting the GluN2A NMDA receptor subunit.
Therapeutic strategies involving alpha-synuclein antibodies show potential for counteracting synaptic dysfunction in Parkinson's disease.