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1.  INFLAMMATORY EFFECTS OF HIGHLY PATHOGENIC H5N1 INFLUENZA VIRUS INFECTION IN THE CNS OF MICE 
The Journal of Neuroscience  2012;32(5):1545-1559.
The A/VN/1203/04 H5N1 influenza virus is capable of infecting the CNS of mice and inducing a number of neurodegenerative pathologies. Here, we examined the effects of H5N1 on several pathological aspects affected in parkinsonism, including loss of the phenotype of dopaminergic (DAergic) neurons located in the substantia nigra pars compacta (SNpc), expression of mono- and indolamines in brain, alterations in SNpc microglia number and morphology, and expression of cytokines, chemokines and growth factors. We find that H5N1 induces a transient loss of the DAergic phenotype in SNpc and now report that this loss recovers by 90 days post infection (dpi). A similar pattern of loss and recovery was seen in monoamine levels of the basal ganglia. The inflammatory response in lung and different regions of the brain known to be targets of the H5N1 virus (brainstem, substantia nigra, striatum, and cortex) were examined at 3, 10, 21, 60 and 90 dpi. We found a significant increase in the number of activated microglia in each of these brain regions that lasted at least 90 days. We also quantified expression of IL-1α, IL-1β, IL-2, IL-6, IL-9, IL-10, IL-12(p70), IL-13, TNF-α, IFN-γ, GM-CSF, G-CSF, M-CSF, eotaxin, IP-10, KC, MCP-1, MIP-1α, MIP-1β and VEGF and find that the pattern and levels of expression are dependent on both brain region and time after infection. We conclude that H5N1 infection in mice induces a long-lasting inflammatory response in brain and may play a contributing factor in the development of pathologies in neurodegenerative disorders.
doi:10.1523/JNEUROSCI.5123-11.2012
PMCID: PMC3307392  PMID: 22302798
2.  Alterations in Glutathione S-transferase pi expression following exposure to MPP+-induced oxidative stress in blood of Parkinson’s disease patients 
Parkinsonism & related disorders  2011;17(10):765-768.
The major motor symptoms of Parkinson’s disease do not occur until a majority of the dopaminergic neurons in the midbrain SNpc have already died. For this reason, it is critical to identify biomarkers that will allow for the identification of presymptomatic individuals. In this study, we examine the baseline expression of the antioxidant protein Glutathione S-transferase pi (GSTpi) in blood of PD and environmental and age-matched controls and compare it to GSTpi levels following exposure to 1-methyl-4-phenylpyridinium (MPP+), an agent that has been shown to induce oxidative stress. We find that 4 hours of exposure to MPP+, significant increases in GSTpi levels can be observed in the leukocytes of PD patients. No changes were seen in other blood components. This suggests that GSTpi and potentially other members of this and other anti-oxidant families may be viable biomarkers for PD.
doi:10.1016/j.parkreldis.2011.06.026
PMCID: PMC3307132  PMID: 21840241

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