The Contribution of α-Synuclein Spreading to Parkinson’s Disease Synaptopathy
Synaptopathies are diseases with synapse defects as shared pathogenic features, encompassing neurodegenerative disorders such as Parkinson’s disease (PD). In sporadic PD, the most common age-related neurodegenerative movement disorder, nigrostriatal dopaminergic deficits are responsible for the onse...
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| Format: | Article |
| Language: | English |
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Wiley
2017-01-01
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| Series: | Neural Plasticity |
| Online Access: | http://dx.doi.org/10.1155/2017/5012129 |
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| author | Francesca Longhena Gaia Faustini Cristina Missale Marina Pizzi PierFranco Spano Arianna Bellucci |
| author_facet | Francesca Longhena Gaia Faustini Cristina Missale Marina Pizzi PierFranco Spano Arianna Bellucci |
| author_sort | Francesca Longhena |
| collection | DOAJ |
| description | Synaptopathies are diseases with synapse defects as shared pathogenic features, encompassing neurodegenerative disorders such as Parkinson’s disease (PD). In sporadic PD, the most common age-related neurodegenerative movement disorder, nigrostriatal dopaminergic deficits are responsible for the onset of motor symptoms that have been related to α-synuclein deposition at synaptic sites. Indeed, α-synuclein accumulation can impair synaptic dopamine release and induces the death of nigrostriatal neurons. While in physiological conditions the protein can interact with and modulate synaptic vesicle proteins and membranes, numerous experimental evidences have confirmed that its pathological aggregation can compromise correct neuronal functioning. In addition, recent findings indicate that α-synuclein pathology spreads into the brain and can affect the peripheral autonomic and somatic nervous system. Indeed, monomeric, oligomeric, and fibrillary α-synuclein can move from cell to cell and can trigger the aggregation of the endogenous protein in recipient neurons. This novel “prion-like” behavior could further contribute to synaptic failure in PD and other synucleinopathies. This review describes the major findings supporting the occurrence of α-synuclein pathology propagation in PD and discusses how this phenomenon could induce or contribute to synaptic injury and degeneration. |
| format | Article |
| id | doaj-art-bbf70845c07c4a82832b2f4a0f7ab625 |
| institution | Kabale University |
| issn | 2090-5904 1687-5443 |
| language | English |
| publishDate | 2017-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Neural Plasticity |
| spelling | doaj-art-bbf70845c07c4a82832b2f4a0f7ab6252025-02-03T05:51:54ZengWileyNeural Plasticity2090-59041687-54432017-01-01201710.1155/2017/50121295012129The Contribution of α-Synuclein Spreading to Parkinson’s Disease SynaptopathyFrancesca Longhena0Gaia Faustini1Cristina Missale2Marina Pizzi3PierFranco Spano4Arianna Bellucci5Department of Molecular and Translational Medicine, University of Brescia, Brescia, ItalyDepartment of Molecular and Translational Medicine, University of Brescia, Brescia, ItalyDepartment of Molecular and Translational Medicine, University of Brescia, Brescia, ItalyDepartment of Molecular and Translational Medicine, University of Brescia, Brescia, ItalyIRCCS Fondazione Ospedale San Camillo (NHS-Italy), Venice Lido, ItalyDepartment of Molecular and Translational Medicine, University of Brescia, Brescia, ItalySynaptopathies are diseases with synapse defects as shared pathogenic features, encompassing neurodegenerative disorders such as Parkinson’s disease (PD). In sporadic PD, the most common age-related neurodegenerative movement disorder, nigrostriatal dopaminergic deficits are responsible for the onset of motor symptoms that have been related to α-synuclein deposition at synaptic sites. Indeed, α-synuclein accumulation can impair synaptic dopamine release and induces the death of nigrostriatal neurons. While in physiological conditions the protein can interact with and modulate synaptic vesicle proteins and membranes, numerous experimental evidences have confirmed that its pathological aggregation can compromise correct neuronal functioning. In addition, recent findings indicate that α-synuclein pathology spreads into the brain and can affect the peripheral autonomic and somatic nervous system. Indeed, monomeric, oligomeric, and fibrillary α-synuclein can move from cell to cell and can trigger the aggregation of the endogenous protein in recipient neurons. This novel “prion-like” behavior could further contribute to synaptic failure in PD and other synucleinopathies. This review describes the major findings supporting the occurrence of α-synuclein pathology propagation in PD and discusses how this phenomenon could induce or contribute to synaptic injury and degeneration.http://dx.doi.org/10.1155/2017/5012129 |
| spellingShingle | Francesca Longhena Gaia Faustini Cristina Missale Marina Pizzi PierFranco Spano Arianna Bellucci The Contribution of α-Synuclein Spreading to Parkinson’s Disease Synaptopathy Neural Plasticity |
| title | The Contribution of α-Synuclein Spreading to Parkinson’s Disease Synaptopathy |
| title_full | The Contribution of α-Synuclein Spreading to Parkinson’s Disease Synaptopathy |
| title_fullStr | The Contribution of α-Synuclein Spreading to Parkinson’s Disease Synaptopathy |
| title_full_unstemmed | The Contribution of α-Synuclein Spreading to Parkinson’s Disease Synaptopathy |
| title_short | The Contribution of α-Synuclein Spreading to Parkinson’s Disease Synaptopathy |
| title_sort | contribution of α synuclein spreading to parkinson s disease synaptopathy |
| url | http://dx.doi.org/10.1155/2017/5012129 |
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