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Animal Models of Parkinson's Disease
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Animal Models of Parkinson's Disease

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: closed (28 February 2022) | Viewed by 35008

Special Issue Editor

Dr. Michele Morari

E-Mail Website
Guest Editor
Department of Medical Sciences, Section of Pharmacology, University of Ferrara, Ferrara, Italy
Interests: Parkinson disease
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

More than two centuries after its first clinical description, Parkinson’s disease remains a major burden for individuals and society and a challenge for clinicians and investigators. Parkinson’s disease is a progressive, multisystemic, multifactorial neurodegenerative disorder, heterogeneously presenting with classical motor symptoms accompanied by non-motor symptoms affecting cognitive, affective, sensory, and autonomic functions. Although pharmacotherapy can achieve a good control over the motor symptoms, no therapy can slow or halt disease progression, revealing our poor understanding of the mechanisms underlying this pathology. The main neuropathological hallmarks of Parkinson’s disease are the loss of dopaminergic neurons in midbrain substantia nigra compacta and the deposition of α-synuclein-positive aggregates, known as Lewy bodies. Nonetheless, the pathology begins in non-dopaminergic neurons years before its diagnosis and slowly spreads throughout the brain via a process whereby neuron–neuron transmission of pathogenic forms of α-synuclein plays a central role. The contribution of genetics to Parkinson’s disease etiology is increasingly recognized, and the number of genetic risk factors is steadily growing. Besides well-established cell-autonomous and -non-autonomous neurotoxic mechanisms (dysregulated mitochondrial activity, protein quality control, and vesicle trafficking, increased oxidative burden, neuroinflammation, excitotoxicity), α-synuclein fibrillization, peripheral inflammation, and gut dysbiosis have emerged as novel potentially targetable processes. Nonetheless, the contribution of these pathways, particularly in the asymptomatic/prodromal phases, remains uncertain. Therefore, the complexity of Parkinson’s disease etio-pathogenesis, the lack of validated biomarkers, and the unmet clinical needs (disease-modifying drugs, drugs for non-motor symptoms, and strategies to manage complications of levodopa pharmacotherapy) urge the validation/refinement of etiological models alongside or “fused” with more classical neurotoxic or genetic models. This Special Issue aims at describing the pros and cons of state-of-the-art in vivo models of Parkinson’s disease and their construct, face, and predictive validity. Both review and research articles are cordially invited.

Dr. Michele Morari
Guest Editor

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Keywords

  • α-synuclein
  • fibrils
  • dyskinesia
  • non-motor symptoms
  • synucleinopathy
  • LRRK2
  • Parkin
  • MPTP
  • autophagy
  • mitochondria

Published Papers (10 papers)

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Research

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16 pages, 3680 KiB  
Article
Dopamine Transporter, PhosphoSerine129 α-Synuclein and α-Synuclein Levels in Aged LRRK2 G2019S Knock-In and Knock-Out Mice
by Chiara Domenicale, Daniela Mercatelli, Federica Albanese, Salvatore Novello, Fabrizio Vincenzi, Katia Varani and Michele Morari
Biomedicines 2022, 10(4), 881; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines10040881 - 12 Apr 2022
Cited by 5 | Viewed by 2405
Abstract
The G2019S mutation in leucine rich-repeat kinase 2 (LRRK2) is a major cause of familial Parkinson’s disease. We previously reported that G2019S knock-in mice manifest dopamine transporter dysfunction and phosphoSerine129 α-synuclein (pSer129 α-syn) immunoreactivity elevation at 12 months of age, which might represent [...] Read more.
The G2019S mutation in leucine rich-repeat kinase 2 (LRRK2) is a major cause of familial Parkinson’s disease. We previously reported that G2019S knock-in mice manifest dopamine transporter dysfunction and phosphoSerine129 α-synuclein (pSer129 α-syn) immunoreactivity elevation at 12 months of age, which might represent pathological events leading to neuronal degeneration. Here, the time-dependence of these changes was monitored in the striatum of 6, 9, 12, 18 and 23-month-old G2019S KI mice and wild-type controls using DA uptake assay, Western analysis and immunohistochemistry. Western analysis showed elevation of membrane dopamine transporter (DAT) levels at 9 and 12 months of age, along with a reduction of vesicular monoamine transporter 2 (VMAT2) levels at 12 months. DAT uptake was abnormally elevated from 9 to up to 18 months. DAT and VMAT2 level changes were specific to the G2019S mutation since they were not observed in LRRK2 kinase-dead or knock-out mice. Nonetheless, dysfunctional DAT uptake was not normalized by acute pharmacological inhibition of LRRK2 kinase activity with MLi-2. Immunoblot analysis showed elevation of pSer129 α-syn levels in the striatum of 12-month-old G2019S KI mice, which, however, was not confirmed by immunohistochemical analysis. Instead, total α-syn immunoreactivity was found elevated in the striatum of 23-month-old LRRK2 knock-out mice. These data indicate mild changes in DA transporters and α-syn metabolism in the striatum of 12-month-old G2019S KI mice whose pathological relevance remains to be established. Full article
(This article belongs to the Special Issue Animal Models of Parkinson's Disease)
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13 pages, 10506 KiB  
Article
Assessment of Repetitive and Compulsive Behaviors Induced by Pramipexole in Rats: Effect of Alpha-Synuclein-Induced Nigrostriatal Degeneration
by Mélina Decourt, Eric Balado, Haritz Jiménez-Urbieta, Maureen Francheteau, Pierre-Olivier Fernagut and Marianne Benoit-Marand
Biomedicines 2022, 10(3), 542; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines10030542 - 24 Feb 2022
Cited by 1 | Viewed by 1838
Abstract
Treatment with dopamine agonists in Parkinson’s disease (PD) is associated with debilitating neuropsychiatric side-effects characterized by impulsive and compulsive behaviors. The vulnerability to develop such impairments is thought to involve interactions between individual vulnerability traits, types of antiparkinsonian medications, and the neurodegenerative process. [...] Read more.
Treatment with dopamine agonists in Parkinson’s disease (PD) is associated with debilitating neuropsychiatric side-effects characterized by impulsive and compulsive behaviors. The vulnerability to develop such impairments is thought to involve interactions between individual vulnerability traits, types of antiparkinsonian medications, and the neurodegenerative process. We investigated the effect of the dopamine D3/D2 agonist pramipexole (PPX) and selective nigrostriatal degeneration achieved by viral-mediated expression of alpha-synuclein on the expression of repetitive and compulsive-like behaviors in rats. In a task assessing spontaneous food hoarding behavior, PPX increased the time spent interacting with food pellets at the expense of hoarding. This disruption of hoarding behavior was identical in sham and lesioned rats. In an operant post-training signal attenuation task, the combination of nigrostriatal lesion and PPX decreased the number of completed trials and increased the number of uncompleted trials. The lesion led to an increased compulsive behavior after signal attenuation, and PPX shifted the overall behavioral output towards an increased proportion of compulsive lever-presses. Given the magnitude of the behavioral effects and the lack of strong interaction between PPX and nigral degeneration, these results suggest that extra-nigral pathology may be critical to increase the vulnerability to develop compulsive behaviors following treatment with D3/D2 agonists. Full article
(This article belongs to the Special Issue Animal Models of Parkinson's Disease)
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16 pages, 3220 KiB  
Article
α-Synuclein Overexpression Increases Dopamine D2/3 Receptor Binding and Immune Activation in a Model of Early Parkinson’s Disease
by Kathrine Stokholm, Majken Borup Thomsen, Jenny-Ann Phan, Line K. Møller, Cecilie Bay-Richter, Søren H. Christiansen, David P. D. Woldbye, Marina Romero-Ramos and Anne M. Landau
Biomedicines 2021, 9(12), 1876; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines9121876 - 10 Dec 2021
Cited by 5 | Viewed by 3244
Abstract
Progressive degeneration of dopaminergic neurons, immune activation, and α-synuclein pathology characterize Parkinson’s disease (PD). We previously reported that unilateral intranigral injection of recombinant adeno-associated viral (rAAV) vectors encoding wild-type human α-synuclein produced a rat model of early PD with dopamine terminal dysfunction. Here [...] Read more.
Progressive degeneration of dopaminergic neurons, immune activation, and α-synuclein pathology characterize Parkinson’s disease (PD). We previously reported that unilateral intranigral injection of recombinant adeno-associated viral (rAAV) vectors encoding wild-type human α-synuclein produced a rat model of early PD with dopamine terminal dysfunction. Here we tested the hypothesis that decreases in dopamine result in increased postsynaptic dopamine D2/D3 receptor expression, neuroinflammation, and reduced synaptic vesicle glycoprotein 2A (SV2A) density. Rats were injected with rAAV encoding α-synuclein or green fluorescent protein and subjected to non-pharmacological motor tests, before euthanization at 12 weeks post-injection. We performed: (1) in situ hybridization of nigral tyrosine hydroxylase mRNA, (2) HPLC of striatal dopamine content, and (3) autoradiography with [3H]raclopride, [3H]DTBZ, [3H]GBR12935, [3H]PK11195, and [3H]UCB-J to measure binding at D2/3 receptors, vesicular monoamine transporter 2, dopamine transporters, mitochondrial translocator protein, and SV2A, respectively. rAAV-α-synuclein induced motor asymmetry and reduced tyrosine hydroxylase mRNA and dopamine content in ipsilateral brain regions. This was paralleled by elevated ipsilateral postsynaptic dopamine D2/3 receptor expression and immune activation, with no changes to synaptic SV2A density. In conclusion, α-synuclein overexpression results in dopaminergic degeneration that induced compensatory increases in D2/3 binding and immune activation, recapitulating many of the pathological characteristics of PD. Full article
(This article belongs to the Special Issue Animal Models of Parkinson's Disease)
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19 pages, 1535 KiB  
Article
A Guide to the Generation of a 6-Hydroxydopamine Mouse Model of Parkinson’s Disease for the Study of Non-Motor Symptoms
by Débora Masini, Carina Plewnia, Maëlle Bertho, Nicolas Scalbert, Vittorio Caggiano and Gilberto Fisone
Biomedicines 2021, 9(6), 598; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines9060598 - 25 May 2021
Cited by 18 | Viewed by 5682
Abstract
In Parkinson’s disease (PD), a large number of symptoms affecting the peripheral and central nervous system precede, develop in parallel to, the cardinal motor symptoms of the disease. The study of these conditions, which are often refractory to and may even be exacerbated [...] Read more.
In Parkinson’s disease (PD), a large number of symptoms affecting the peripheral and central nervous system precede, develop in parallel to, the cardinal motor symptoms of the disease. The study of these conditions, which are often refractory to and may even be exacerbated by standard dopamine replacement therapies, relies on the availability of appropriate animal models. Previous work in rodents showed that injection of the neurotoxin 6-hydroxydopamine (6-OHDA) in discrete brain regions reproduces several non-motor comorbidities commonly associated with PD, including cognitive deficits, depression, anxiety, as well as disruption of olfactory discrimination and circadian rhythm. However, the use of 6-OHDA is frequently associated with significant post-surgical mortality. Here, we describe the generation of a mouse model of PD based on bilateral injection of 6-OHDA in the dorsal striatum. We show that the survival rates of males and females subjected to this lesion differ significantly, with a much higher mortality among males, and provide a protocol of enhanced pre- and post-operative care, which nearly eliminates animal loss. We also briefly discuss the utility of this model for the study of non-motor comorbidities of PD. Full article
(This article belongs to the Special Issue Animal Models of Parkinson's Disease)
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15 pages, 23381 KiB  
Article
Early Dysfunction of Substantia Nigra Dopamine Neurons in the ParkinQ311X Mouse
by Maria Regoni, Letizia Zanetti, Stefano Comai, Daniela Mercatelli, Salvatore Novello, Federica Albanese, Laura Croci, Gian Giacomo Consalez, Andrea Ciammola, Flavia Valtorta, Michele Morari and Jenny Sassone
Biomedicines 2021, 9(5), 514; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines9050514 - 05 May 2021
Cited by 4 | Viewed by 2820
Abstract
Mutations in the PARK2 gene encoding the protein parkin cause autosomal recessive juvenile parkinsonism (ARJP), a neurodegenerative disease characterized by early dysfunction and loss of dopamine (DA) neurons in the substantia nigra pars compacta (SNc). No therapy is currently available to prevent or [...] Read more.
Mutations in the PARK2 gene encoding the protein parkin cause autosomal recessive juvenile parkinsonism (ARJP), a neurodegenerative disease characterized by early dysfunction and loss of dopamine (DA) neurons in the substantia nigra pars compacta (SNc). No therapy is currently available to prevent or slow down the neurodegeneration in ARJP patients. Preclinical models are key to clarifying the early events that lead to neurodegeneration and reveal the potential of novel neuroprotective strategies. ParkinQ311X is a transgenic mouse model expressing in DA neurons a mutant parkin variant found in ARJP patients. This model was previously reported to show the neuropathological hallmark of the disease, i.e., the progressive loss of DA neurons. However, the early dysfunctions that precede neurodegeneration have never been investigated. Here, we analyzed SNc DA neurons in parkinQ311X mice and found early features of mitochondrial dysfunction, extensive cytoplasmic vacuolization, and dysregulation of spontaneous in vivo firing activity. These data suggest that the parkinQ311X mouse recapitulates key features of ARJP and provides a useful tool for studying the neurodegenerative mechanisms underlying the human disease and for screening potential neuroprotective drugs. Full article
(This article belongs to the Special Issue Animal Models of Parkinson's Disease)
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14 pages, 2694 KiB  
Article
Oral Administration of Probiotic Bifidobacterium breve Improves Facilitation of Hippocampal Memory Extinction via Restoration of Aberrant Higher Induction of Neuropsin in an MPTP-Induced Mouse Model of Parkinson’s Disease
by Toshiaki Ishii, Hidefumi Furuoka, Motohiro Kaya and Tetsuya Kuhara
Biomedicines 2021, 9(2), 167; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines9020167 - 08 Feb 2021
Cited by 21 | Viewed by 3538
Abstract
We previously reported that 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced Parkinson’s disease (PD) model mice (PD mice) facilitate hippocampal memory extinction, which may be the cause of cognitive impairment in PD. Recent studies on the consumption of probiotics have reported a variety of beneficial effects on the central [...] Read more.
We previously reported that 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced Parkinson’s disease (PD) model mice (PD mice) facilitate hippocampal memory extinction, which may be the cause of cognitive impairment in PD. Recent studies on the consumption of probiotics have reported a variety of beneficial effects on the central nervous system via the microbiota–gut–brain axis. In this study, we investigated the effects of oral administration of Bifidobacterium breve strain A1 [MCC1274] (B. breve A1) on the facilitation of hippocampal memory extinction observed in PD mice. We found that four-day consecutive oral administration of B. breve A1 restored facilitation of contextual fear extinction in PD mice. Hippocampal mRNA expression levels of postsynaptic density protein-95 and synaptophysin significantly decreased in the PD mice, but mRNA and protein expression levels of neuropsin increased. Furthermore, CA1 apical spine density was significantly reduced in PD mice. On the other hand, administration of B. breve A1 to PD mice recovered all these expression levels and the CA1 spine density to control levels. These results suggest that increased induction of neuropsin is involved in abnormal changes in hippocampal synaptic plasticity, and that B. breve A1 imposes reins on its expression, resulting in the restoration of abnormal hippocampal synaptic plasticity and the facilitation of fear extinction in PD mice. Full article
(This article belongs to the Special Issue Animal Models of Parkinson's Disease)
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Review

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53 pages, 2201 KiB  
Review
Animal Models of Autosomal Recessive Parkinsonism
by Guendalina Bastioli, Maria Regoni, Federico Cazzaniga, Chiara Maria Giulia De Luca, Edoardo Bistaffa, Letizia Zanetti, Fabio Moda, Flavia Valtorta and Jenny Sassone
Biomedicines 2021, 9(7), 812; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines9070812 - 13 Jul 2021
Cited by 7 | Viewed by 3281
Abstract
Parkinson’s disease (PD) is the most common neurodegenerative movement disorder. The neuropathological hallmark of the disease is the loss of dopamine neurons of the substantia nigra pars compacta. The clinical manifestations of PD are bradykinesia, rigidity, resting tremors and postural instability. PD patients [...] Read more.
Parkinson’s disease (PD) is the most common neurodegenerative movement disorder. The neuropathological hallmark of the disease is the loss of dopamine neurons of the substantia nigra pars compacta. The clinical manifestations of PD are bradykinesia, rigidity, resting tremors and postural instability. PD patients often display non-motor symptoms such as depression, anxiety, weakness, sleep disturbances and cognitive disorders. Although, in 90% of cases, PD has a sporadic onset of unknown etiology, highly penetrant rare genetic mutations in many genes have been linked with typical familial PD. Understanding the mechanisms behind the DA neuron death in these Mendelian forms may help to illuminate the pathogenesis of DA neuron degeneration in the more common forms of PD. A key step in the identification of the molecular pathways underlying DA neuron death, and in the development of therapeutic strategies, is the creation and characterization of animal models that faithfully recapitulate the human disease. In this review, we outline the current status of PD modeling using mouse, rat and non-mammalian models, focusing on animal models for autosomal recessive PD. Full article
(This article belongs to the Special Issue Animal Models of Parkinson's Disease)
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27 pages, 845 KiB  
Review
Neuropsychiatric and Cognitive Deficits in Parkinson’s Disease and Their Modeling in Rodents
by Mélina Decourt, Haritz Jiménez-Urbieta, Marianne Benoit-Marand and Pierre-Olivier Fernagut
Biomedicines 2021, 9(6), 684; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines9060684 - 17 Jun 2021
Cited by 15 | Viewed by 3917
Abstract
Parkinson’s disease (PD) is associated with a large burden of non-motor symptoms including olfactory and autonomic dysfunction, as well as neuropsychiatric (depression, anxiety, apathy) and cognitive disorders (executive dysfunctions, memory and learning impairments). Some of these non-motor symptoms may precede the onset of [...] Read more.
Parkinson’s disease (PD) is associated with a large burden of non-motor symptoms including olfactory and autonomic dysfunction, as well as neuropsychiatric (depression, anxiety, apathy) and cognitive disorders (executive dysfunctions, memory and learning impairments). Some of these non-motor symptoms may precede the onset of motor symptoms by several years, and they significantly worsen during the course of the disease. The lack of systematic improvement of these non-motor features by dopamine replacement therapy underlines their multifactorial origin, with an involvement of monoaminergic and cholinergic systems, as well as alpha-synuclein pathology in frontal and limbic cortical circuits. Here we describe mood and neuropsychiatric disorders in PD and review their occurrence in rodent models of PD. Altogether, toxin-based rodent models of PD indicate a significant but non-exclusive contribution of mesencephalic dopaminergic loss in anxiety, apathy, and depressive-like behaviors, as well as in learning and memory deficits. Gene-based models display significant deficits in learning and memory, as well as executive functions, highlighting the contribution of alpha-synuclein pathology to these non-motor deficits. Collectively, neuropsychiatric and cognitive deficits are recapitulated to some extent in rodent models, providing partial but nevertheless useful options to understand the pathophysiology of non-motor symptoms and develop therapeutic options for these debilitating symptoms of PD. Full article
(This article belongs to the Special Issue Animal Models of Parkinson's Disease)
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13 pages, 1094 KiB  
Review
Dopamine D3 Receptor Plasticity in Parkinson’s Disease and L-DOPA-Induced Dyskinesia
by Kathryn Lanza and Christopher Bishop
Biomedicines 2021, 9(3), 314; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines9030314 - 19 Mar 2021
Cited by 8 | Viewed by 3829
Abstract
Parkinson’s Disease (PD) is characterized by primary and secondary plasticity that occurs in response to progressive degeneration and long-term L-DOPA treatment. Some of this plasticity contributes to the detrimental side effects associated with chronic L-DOPA treatment, namely L-DOPA-induced dyskinesia (LID). The dopamine D3 [...] Read more.
Parkinson’s Disease (PD) is characterized by primary and secondary plasticity that occurs in response to progressive degeneration and long-term L-DOPA treatment. Some of this plasticity contributes to the detrimental side effects associated with chronic L-DOPA treatment, namely L-DOPA-induced dyskinesia (LID). The dopamine D3 receptor (D3R) has emerged as a promising target in LID management as it is upregulated in LID. This upregulation occurs primarily in the D1-receptor-bearing (D1R) cells of the striatum, which have been repeatedly implicated in LID manifestation. D3R undergoes dynamic changes both in PD and in LID, making it difficult to delineate D3R’s specific contributions, but recent genetic and pharmacologic tools have helped to clarify its role in LID. The following review will discuss these changes, recent advances to better clarify D3R in both PD and LID and potential steps for translating these findings. Full article
(This article belongs to the Special Issue Animal Models of Parkinson's Disease)
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18 pages, 609 KiB  
Review
A New Rise of Non-Human Primate Models of Synucleinopathies
by Margaux Teil, Marie-Laure Arotcarena and Benjamin Dehay
Biomedicines 2021, 9(3), 272; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines9030272 - 09 Mar 2021
Cited by 8 | Viewed by 3159
Abstract
Synucleinopathies are neurodegenerative diseases characterized by the presence of α-synuclein-positive intracytoplasmic inclusions in the central nervous system. Multiple experimental models have been extensively used to understand better the mechanisms involved in the pathogenesis of synucleinopathy. Non-human primate (NHP) models are of interest in [...] Read more.
Synucleinopathies are neurodegenerative diseases characterized by the presence of α-synuclein-positive intracytoplasmic inclusions in the central nervous system. Multiple experimental models have been extensively used to understand better the mechanisms involved in the pathogenesis of synucleinopathy. Non-human primate (NHP) models are of interest in neurodegenerative diseases as they constitute the highest relevant preclinical model in translational research. They also contribute to bringing new insights into synucleinopathy’s pathogenicity and help in the quest and validation of therapeutical strategies. Here, we reviewed the different NHP models that have recapitulated key characteristics of synucleinopathy, and we aimed to highlight the contribution of NHP in mechanistic and translational approaches for synucleinopathies. Full article
(This article belongs to the Special Issue Animal Models of Parkinson's Disease)
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