Centrality of Early Synaptopathy in Parkinson's Disease

Paola Imbriani, Tommaso Schirinzi, Maria Meringolo, Nicola B Mercuri, Antonio Pisani

Research output: Contribution to journalReview article

Abstract

Significant advances have been made in the understanding of the numerous mechanisms involved in Parkinson's disease (PD) pathogenesis. The identification of PD pathogenic mutations and the use of different animal models have contributed to better elucidate the processes underlying the disease. Here, we report a brief survey of some relevant cellular mechanisms, including autophagic-lysosomal dysfunction, endoplasmic reticulum stress, and mitochondrial impairment, with the main aim to focus on their potential convergent roles in determining early alterations at the synaptic level, mainly consisting in a decrease in dopamine release at nigrostriatal terminals and loss of synaptic plasticity at corticostriatal synapses. In a number of experimental models, this synaptopathy has been shown to be an initial, central event in PD pathogenesis, preceding neuronal damage, thereby representing a valuable tool for testing potential disease-modifying treatments.

Original languageEnglish
Pages (from-to)103
JournalFrontiers in Neurology
Volume9
DOIs
Publication statusPublished - 2018

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Parkinson Disease
Endoplasmic Reticulum Stress
Neuronal Plasticity
Synapses
Dopamine
Theoretical Models
Animal Models
Mutation
Surveys and Questionnaires

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Centrality of Early Synaptopathy in Parkinson's Disease. / Imbriani, Paola; Schirinzi, Tommaso; Meringolo, Maria; Mercuri, Nicola B; Pisani, Antonio.

In: Frontiers in Neurology, Vol. 9, 2018, p. 103.

Research output: Contribution to journalReview article

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