2010
DOI: 10.1016/j.parkreldis.2009.05.005
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[11C]-PK11195 PET: Quantification of neuroinflammation and a monitor of anti-inflammatory treatment in Parkinson's disease?

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Cited by 162 publications
(113 citation statements)
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“…Whereas results of previous PET studies using 11 C-PK11195 in Parkinson's disease showed increased binding in the midbrain 35 and different frontal and temporal cortical regions, 36 other reports did not identify major differences between binding in Parkinson's disease and controls. 37 Conversely, more consistent increases in 11 C-PK11195 binding have been reported in multiple systems atrophy, 38 progressive supranuclear palsy, 39 corticobasal degeneration, 40 and Huntington's disease. 41 Reasons for such variability could include limitations inherent to this particular tracer, such as high non-specific binding, low brainpenetration, high plasma-protein-binding, and difficult preparation.…”
Section: Neuroinflammationmentioning
confidence: 92%
“…Whereas results of previous PET studies using 11 C-PK11195 in Parkinson's disease showed increased binding in the midbrain 35 and different frontal and temporal cortical regions, 36 other reports did not identify major differences between binding in Parkinson's disease and controls. 37 Conversely, more consistent increases in 11 C-PK11195 binding have been reported in multiple systems atrophy, 38 progressive supranuclear palsy, 39 corticobasal degeneration, 40 and Huntington's disease. 41 Reasons for such variability could include limitations inherent to this particular tracer, such as high non-specific binding, low brainpenetration, high plasma-protein-binding, and difficult preparation.…”
Section: Neuroinflammationmentioning
confidence: 92%
“…Recent evidence suggests that neurodegenerative disorders such as Alzheimer's and Parkinson's diseases (and interestingly also schizophrenia), are also associated with chronic neuroinflammation [100,101]. Chronic neurodegeneration is associated with morphological and cell surface marker evidence of selective activation of microglial cells, but only minimal pro-inflammatory cytokine synthesis [102].…”
Section: Neurodegeneration As a Cause Of Primingmentioning
confidence: 99%
“…Activation of microglia is associated with expression of peripheral benzodiazepine receptor on mitochondria. This receptor is selectively expressed in the mitochondrial walls of activated microglia [100,101], and thus positron-emission tomography scanning with 11 C-PK11195 can provide a quantitative assay of cerebral inflammation. Other positron-emission tomography modalities that may provide important information include functional methods for assessing cerebral glucose metabolism (e.g.…”
Section: The Futurementioning
confidence: 99%
“…Pathologic changes in the PD brain are closely related to microglial activation induced inflammation, which accelerates dopamine (DA)-producing neuron death. Interestingly, positron emission tomography (PET) studies have shown noticeable microglial activation in the SN, putamen and subcortical and cortical areas of the PD brain [10,11].…”
Section: Relations Between Microglial Activation and Neuronal Cell Dementioning
confidence: 99%