Oxidative stress and synaptic dysfunction in rodent models of Parkinson's disease
Parkinson's disease (PD) is a multifactorial disorder involving a complex interplay between a variety of genetic and environmental factors. In this scenario, mitochondrial impairment and oxidative stress are widely accepted as crucial neuropathogenic mechanisms, as also evidenced by the identif...
| Main Authors: | , , , |
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| Format: | Article |
| Language: | English |
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Elsevier
2022-10-01
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| Series: | Neurobiology of Disease |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S0969996122002431 |
| _version_ | 1811272247144349696 |
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| author | Paola Imbriani Giuseppina Martella Paola Bonsi Antonio Pisani |
| author_facet | Paola Imbriani Giuseppina Martella Paola Bonsi Antonio Pisani |
| author_sort | Paola Imbriani |
| collection | DOAJ |
| description | Parkinson's disease (PD) is a multifactorial disorder involving a complex interplay between a variety of genetic and environmental factors. In this scenario, mitochondrial impairment and oxidative stress are widely accepted as crucial neuropathogenic mechanisms, as also evidenced by the identification of PD-associated genes that are directly involved in mitochondrial function. The concept of mitochondrial dysfunction is closely linked to that of synaptic dysfunction. Indeed, compelling evidence supports the role of mitochondria in synaptic transmission and plasticity, although many aspects have not yet been fully elucidated. Here, we will provide a brief overview of the most relevant evidence obtained in different neurotoxin-based and genetic rodent models of PD, focusing on mitochondrial impairment and synaptopathy, an early central event preceding overt nigrostriatal neurodegeneration. The identification of early deficits occurring in PD pathogenesis is crucial in view of the development of potential disease-modifying therapeutic strategies. |
| first_indexed | 2024-04-12T22:36:54Z |
| format | Article |
| id | doaj.art-1a871112b8c24356b53421db41fc344f |
| institution | Directory Open Access Journal |
| issn | 1095-953X |
| language | English |
| last_indexed | 2024-04-12T22:36:54Z |
| publishDate | 2022-10-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Neurobiology of Disease |
| spelling | doaj.art-1a871112b8c24356b53421db41fc344f2022-12-22T03:13:50ZengElsevierNeurobiology of Disease1095-953X2022-10-01173105851Oxidative stress and synaptic dysfunction in rodent models of Parkinson's diseasePaola Imbriani0Giuseppina Martella1Paola Bonsi2Antonio Pisani3Laboratory of Neurophysiology and Plasticity, IRCCS Fondazione Santa Lucia, Rome, ItalyLaboratory of Neurophysiology and Plasticity, IRCCS Fondazione Santa Lucia, Rome, ItalyLaboratory of Neurophysiology and Plasticity, IRCCS Fondazione Santa Lucia, Rome, ItalyDepartment of Brain and Behavioral Sciences, University of Pavia, Pavia, Italy; IRCCS Mondino Foundation, Pavia, Italy; Corresponding author at: Department of Brain and Behavioral Sciences, University of Pavia, IRCCS Mondino Foundation, via Mondino 2, Pavia, Italy.Parkinson's disease (PD) is a multifactorial disorder involving a complex interplay between a variety of genetic and environmental factors. In this scenario, mitochondrial impairment and oxidative stress are widely accepted as crucial neuropathogenic mechanisms, as also evidenced by the identification of PD-associated genes that are directly involved in mitochondrial function. The concept of mitochondrial dysfunction is closely linked to that of synaptic dysfunction. Indeed, compelling evidence supports the role of mitochondria in synaptic transmission and plasticity, although many aspects have not yet been fully elucidated. Here, we will provide a brief overview of the most relevant evidence obtained in different neurotoxin-based and genetic rodent models of PD, focusing on mitochondrial impairment and synaptopathy, an early central event preceding overt nigrostriatal neurodegeneration. The identification of early deficits occurring in PD pathogenesis is crucial in view of the development of potential disease-modifying therapeutic strategies.http://www.sciencedirect.com/science/article/pii/S0969996122002431Parkinson's diseaseMitochondriaOxidative stressStriatumSubstantia nigraDopamine transmission |
| spellingShingle | Paola Imbriani Giuseppina Martella Paola Bonsi Antonio Pisani Oxidative stress and synaptic dysfunction in rodent models of Parkinson's disease Neurobiology of Disease Parkinson's disease Mitochondria Oxidative stress Striatum Substantia nigra Dopamine transmission |
| title | Oxidative stress and synaptic dysfunction in rodent models of Parkinson's disease |
| title_full | Oxidative stress and synaptic dysfunction in rodent models of Parkinson's disease |
| title_fullStr | Oxidative stress and synaptic dysfunction in rodent models of Parkinson's disease |
| title_full_unstemmed | Oxidative stress and synaptic dysfunction in rodent models of Parkinson's disease |
| title_short | Oxidative stress and synaptic dysfunction in rodent models of Parkinson's disease |
| title_sort | oxidative stress and synaptic dysfunction in rodent models of parkinson s disease |
| topic | Parkinson's disease Mitochondria Oxidative stress Striatum Substantia nigra Dopamine transmission |
| url | http://www.sciencedirect.com/science/article/pii/S0969996122002431 |
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