Parkin Deficiency Increases Vulnerability to Inflammation-Related Nigral Degeneration

The loss of nigral dopaminergic (DA) neurons in idiopathic Parkinson's disease (PD) is believed to result from interactions between genetic susceptibility and environmental factors. Evidence that inflammatory processes modulate PD risk comes from prospective studies that suggest that higher pla...

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Veröffentlicht in:The Journal of neuroscience 2008-10, Vol.28 (43), p.10825-10834
Hauptverfasser: Frank-Cannon, Tamy C, Tran, Thi, Ruhn, Kelly A, Martinez, Terina N, Hong, John, Marvin, Marian, Hartley, Meagan, Trevino, Isaac, O'Brien, Daniel E, Casey, Bradford, Goldberg, Matthew S, Tansey, Malu G
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container_end_page 10834
container_issue 43
container_start_page 10825
container_title The Journal of neuroscience
container_volume 28
creator Frank-Cannon, Tamy C
Tran, Thi
Ruhn, Kelly A
Martinez, Terina N
Hong, John
Marvin, Marian
Hartley, Meagan
Trevino, Isaac
O'Brien, Daniel E
Casey, Bradford
Goldberg, Matthew S
Tansey, Malu G
description The loss of nigral dopaminergic (DA) neurons in idiopathic Parkinson's disease (PD) is believed to result from interactions between genetic susceptibility and environmental factors. Evidence that inflammatory processes modulate PD risk comes from prospective studies that suggest that higher plasma concentrations of a number of proinflammatory cytokines correlate with an increased risk of developing PD and chronic nonsteroidal anti-inflammatory drug regimens reduce the incidence of PD. Although loss-of-function mutations in the parkin gene cause early-onset familial PD, Parkin-deficient (parkin-/-) mice do not display nigrostriatal pathway degeneration, suggesting that a genetic factor is not sufficient, and an environmental trigger may be needed to cause nigral DA neuron loss. To test the hypothesis that parkin-/- mice require an inflammatory stimulus to develop nigral DA neuron loss, low-dose lipopolysaccaride (LPS) was administered intraperitoneally for prolonged periods. Quantitative real-time PCR and immunofluorescence labeling of inflammatory markers indicated that this systemic LPS treatment regimen triggered persistent neuroinflammation in wild-type and parkin-/- mice. Although inflammatory and oxidative stress responses to the inflammation regimen did not differ significantly between the two genotypes, only parkin-/- mice displayed subtle fine-motor deficits and selective loss of DA neurons in substantia nigra. Therefore, our studies suggest that loss of Parkin function increases the vulnerability of nigral DA neurons to inflammation-related degeneration. This new model of nigral DA neuron loss may enable identification of early biomarkers of degeneration and aid in preclinical screening efforts to identify compounds that can halt or delay the progressive degeneration of the nigrostriatal pathway.
doi_str_mv 10.1523/JNEUROSCI.3001-08.2008
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Evidence that inflammatory processes modulate PD risk comes from prospective studies that suggest that higher plasma concentrations of a number of proinflammatory cytokines correlate with an increased risk of developing PD and chronic nonsteroidal anti-inflammatory drug regimens reduce the incidence of PD. Although loss-of-function mutations in the parkin gene cause early-onset familial PD, Parkin-deficient (parkin-/-) mice do not display nigrostriatal pathway degeneration, suggesting that a genetic factor is not sufficient, and an environmental trigger may be needed to cause nigral DA neuron loss. To test the hypothesis that parkin-/- mice require an inflammatory stimulus to develop nigral DA neuron loss, low-dose lipopolysaccaride (LPS) was administered intraperitoneally for prolonged periods. Quantitative real-time PCR and immunofluorescence labeling of inflammatory markers indicated that this systemic LPS treatment regimen triggered persistent neuroinflammation in wild-type and parkin-/- mice. Although inflammatory and oxidative stress responses to the inflammation regimen did not differ significantly between the two genotypes, only parkin-/- mice displayed subtle fine-motor deficits and selective loss of DA neurons in substantia nigra. Therefore, our studies suggest that loss of Parkin function increases the vulnerability of nigral DA neurons to inflammation-related degeneration. 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Quantitative real-time PCR and immunofluorescence labeling of inflammatory markers indicated that this systemic LPS treatment regimen triggered persistent neuroinflammation in wild-type and parkin-/- mice. Although inflammatory and oxidative stress responses to the inflammation regimen did not differ significantly between the two genotypes, only parkin-/- mice displayed subtle fine-motor deficits and selective loss of DA neurons in substantia nigra. Therefore, our studies suggest that loss of Parkin function increases the vulnerability of nigral DA neurons to inflammation-related degeneration. 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subjects Animals
Behavior, Animal - drug effects
Cell Survival - drug effects
Cytokines - metabolism
Dopamine - metabolism
Exploratory Behavior - drug effects
Exploratory Behavior - physiology
Gait Disorders, Neurologic - etiology
Gait Disorders, Neurologic - genetics
Heme Oxygenase-1 - genetics
Heme Oxygenase-1 - metabolism
Inflammation - chemically induced
Inflammation - complications
Mice
Mice, Knockout
Motor Activity - drug effects
Motor Activity - genetics
Multivariate Analysis
Nerve Degeneration - etiology
Nerve Degeneration - metabolism
NF-E2-Related Factor 2 - genetics
NF-E2-Related Factor 2 - metabolism
Nitric Oxide Synthase Type II - genetics
Nitric Oxide Synthase Type II - metabolism
Polysaccharides
Psychomotor Performance - drug effects
Psychomotor Performance - physiology
Rotarod Performance Test
Substantia Nigra - metabolism
Substantia Nigra - pathology
Superoxide Dismutase - genetics
Superoxide Dismutase - metabolism
Tyrosine 3-Monooxygenase
Ubiquitin-Protein Ligases - deficiency
title Parkin Deficiency Increases Vulnerability to Inflammation-Related Nigral Degeneration
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