Progressive Neurodegeneration or Endogenous Compensation in an Animal Model of Parkinson's Disease Produced by Decreasing Doses of Alpha-Synuclein
Identifieur interne : 001610 ( Main/Exploration ); précédent : 001609; suivant : 001611Progressive Neurodegeneration or Endogenous Compensation in an Animal Model of Parkinson's Disease Produced by Decreasing Doses of Alpha-Synuclein
Auteurs : James B. Koprich ; Tom H. Johnston ; Philippe Huot ; M. Gabriela Reyes ; Maria Espinosa ; Jonathan M. BrotchieSource :
- PLoS ONE [ 1932-6203 ] ; 2011.
English descriptors
- KwdEn :
- Animals, Axons (pathology), Cell Count, Dependovirus (genetics), Disease Models, Animal, Dopamine Plasma Membrane Transport Proteins (metabolism), Female, Forelimb, Genetic Therapy, Genetic Vectors, Neostriatum (metabolism), Neostriatum (pathology), Nerve Degeneration (pathology), Parkinson Disease (pathology), Parkinson Disease (therapy), Prosencephalon (metabolism), Prosencephalon (pathology), Protein Transport, Rats, Rats, Sprague-Dawley, Substantia Nigra (enzymology), Substantia Nigra (pathology), Transgenes (genetics), Tyrosine 3-Monooxygenase (metabolism), alpha-Synuclein (genetics), alpha-Synuclein (therapeutic use).
- MESH :
- chemical , genetics : alpha-Synuclein.
- chemical , metabolism : Dopamine Plasma Membrane Transport Proteins, Tyrosine 3-Monooxygenase.
- enzymology : Substantia Nigra.
- genetics : Dependovirus, Transgenes.
- metabolism : Neostriatum, Prosencephalon.
- pathology : Axons, Neostriatum, Nerve Degeneration, Parkinson Disease, Prosencephalon, Substantia Nigra.
- chemical , therapeutic use : alpha-Synuclein.
- therapy : Parkinson Disease.
- Animals, Cell Count, Disease Models, Animal, Female, Forelimb, Genetic Therapy, Genetic Vectors, Protein Transport, Rats, Rats, Sprague-Dawley.
Abstract
The pathological hallmarks of Parkinson's disease (PD) are degeneration of dopamine (DA) neurons of the substantia nigra (SN) and the presence of alpha-synuclein (α-syn)-rich Lewy bodies in DA cells that remain. To model these aspects of the disease, we previously showed that high titer (5.1×10exp12 gp/ml) AAV1/2 driven expression of A53T α-syn in the SN of rats caused nigrostriatal pathology including a loss of DA neurons, but also with toxicity in the GFP control group. In the current study, we evaluate the effects of two lower titers by dilution of the vector (1∶3 [1.7×10exp12] and 1∶10 [5.1×10exp11]) to define a concentration that produced pathology specific for α-syn. In GFP and empty vector groups there were no behavioural or post-mortem changes at 3 or 6 weeks post-administration at either vector dose. Dilution of the AAV1/2 A53T α-syn (1∶3) produced significant paw use asymmetry, reductions in striatal tyrosine hydroxylase (TH), and increases in DA turnover at 3 weeks in the absence of overt pathology. By 6 weeks greater evidence of pathology was observed and included, reductions in SN DA neurons, striatal DA, TH and DA-transporter, along with a sustained behavioural deficit. In contrast, the 1∶10 AAV1/2 A53T α-syn treated animals showed normalization between 3 and 6 weeks in paw use asymmetry, reductions in striatal TH, and increased DA turnover. Progression of dopaminergic deficits using the 1∶3 titer of AAV1/2 A53Tα-syn provides a platform for evaluating treatments directed at preventing and/or reversing synucleinopathy. Use of the 1∶10 titer of AAV1/2 A53T α-syn provides an opportunity to study mechanisms of endogenous compensation. Furthermore, these data highlight the need to characterize the titer of vector being utilized, when using AAV to express pathogenic proteins and model disease process, to avoid producing non-specific effects.
Url:
DOI: 10.1371/journal.pone.0017698
PubMed: 21408191
PubMed Central: 3049796
Affiliations:
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<term>Cell Count</term>
<term>Dependovirus (genetics)</term>
<term>Disease Models, Animal</term>
<term>Dopamine Plasma Membrane Transport Proteins (metabolism)</term>
<term>Female</term>
<term>Forelimb</term>
<term>Genetic Therapy</term>
<term>Genetic Vectors</term>
<term>Neostriatum (metabolism)</term>
<term>Neostriatum (pathology)</term>
<term>Nerve Degeneration (pathology)</term>
<term>Parkinson Disease (pathology)</term>
<term>Parkinson Disease (therapy)</term>
<term>Prosencephalon (metabolism)</term>
<term>Prosencephalon (pathology)</term>
<term>Protein Transport</term>
<term>Rats</term>
<term>Rats, Sprague-Dawley</term>
<term>Substantia Nigra (enzymology)</term>
<term>Substantia Nigra (pathology)</term>
<term>Transgenes (genetics)</term>
<term>Tyrosine 3-Monooxygenase (metabolism)</term>
<term>alpha-Synuclein (genetics)</term>
<term>alpha-Synuclein (therapeutic use)</term>
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<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>alpha-Synuclein</term>
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<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Dopamine Plasma Membrane Transport Proteins</term>
<term>Tyrosine 3-Monooxygenase</term>
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<keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Substantia Nigra</term>
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<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Dependovirus</term>
<term>Transgenes</term>
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<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Neostriatum</term>
<term>Prosencephalon</term>
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<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Axons</term>
<term>Neostriatum</term>
<term>Nerve Degeneration</term>
<term>Parkinson Disease</term>
<term>Prosencephalon</term>
<term>Substantia Nigra</term>
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<term>Genetic Therapy</term>
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<front><div type="abstract" xml:lang="en"><p>The pathological hallmarks of Parkinson's disease (PD) are degeneration of dopamine (DA) neurons of the substantia nigra (SN) and the presence of alpha-synuclein (α-syn)-rich Lewy bodies in DA cells that remain. To model these aspects of the disease, we previously showed that high titer (5.1×10exp12 gp/ml) AAV1/2 driven expression of A53T α-syn in the SN of rats caused nigrostriatal pathology including a loss of DA neurons, but also with toxicity in the GFP control group. In the current study, we evaluate the effects of two lower titers by dilution of the vector (1∶3 [1.7×10exp12] and 1∶10 [5.1×10exp11]) to define a concentration that produced pathology specific for α-syn. In GFP and empty vector groups there were no behavioural or post-mortem changes at 3 or 6 weeks post-administration at either vector dose. Dilution of the AAV1/2 A53T α-syn (1∶3) produced significant paw use asymmetry, reductions in striatal tyrosine hydroxylase (TH), and increases in DA turnover at 3 weeks in the absence of overt pathology. By 6 weeks greater evidence of pathology was observed and included, reductions in SN DA neurons, striatal DA, TH and DA-transporter, along with a sustained behavioural deficit. In contrast, the 1∶10 AAV1/2 A53T α-syn treated animals showed normalization between 3 and 6 weeks in paw use asymmetry, reductions in striatal TH, and increased DA turnover. Progression of dopaminergic deficits using the 1∶3 titer of AAV1/2 A53Tα-syn provides a platform for evaluating treatments directed at preventing and/or reversing synucleinopathy. Use of the 1∶10 titer of AAV1/2 A53T α-syn provides an opportunity to study mechanisms of endogenous compensation. Furthermore, these data highlight the need to characterize the titer of vector being utilized, when using AAV to express pathogenic proteins and model disease process, to avoid producing non-specific effects.</p>
</div>
</front>
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<tree><noCountry><name sortKey="Brotchie, Jonathan M" sort="Brotchie, Jonathan M" uniqKey="Brotchie J" first="Jonathan M." last="Brotchie">Jonathan M. Brotchie</name>
<name sortKey="Espinosa, Maria" sort="Espinosa, Maria" uniqKey="Espinosa M" first="Maria" last="Espinosa">Maria Espinosa</name>
<name sortKey="Huot, Philippe" sort="Huot, Philippe" uniqKey="Huot P" first="Philippe" last="Huot">Philippe Huot</name>
<name sortKey="Johnston, Tom H" sort="Johnston, Tom H" uniqKey="Johnston T" first="Tom H." last="Johnston">Tom H. Johnston</name>
<name sortKey="Koprich, James B" sort="Koprich, James B" uniqKey="Koprich J" first="James B." last="Koprich">James B. Koprich</name>
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