Source 1primary paper2014PLoS ONE
Toolkit/in vivo PET ([(11)C]-PE2I)
in vivo PET ([(11)C]-PE2I)
Taxonomy: Technique Branch / Method. Workflows sit above the mechanism and technique branches rather than replacing them.
Summary
In vivo PET with [(11)C]-PE2I is a radiotracer imaging assay used to assess dopamine degeneration in MPTP-treated non-human primates. In the cited study, it was applied alongside post-mortem tyrosine hydroxylase and dopamine transporter quantification.
Usefulness & Problems
Why this is useful
This assay provides an in vivo readout for dopamine degeneration in a non-human primate MPTP model. Its utility in the supplied evidence is as part of a multimodal assessment combined with post-mortem TH and DAT measurements.
Problem solved
It addresses the need to assess dopaminergic degeneration in living MPTP-treated non-human primates. The evidence does not provide further detail on assay performance metrics or analytical outputs.
Taxonomy & Function
Primary hierarchy
Technique Branch
Method: A concrete measurement method used to characterize an engineered system.
Mechanisms
positron emission tomography imagingpositron emission tomography imagingradiotracer-based detectionradiotracer-based detectionTarget processes
No target processes tagged yet.
Implementation Constraints
cofactor dependency: cofactor requirement unknownencoding mode: genetically encodedimplementation constraint: context specific validationoperating role: sensor
Implementation requires positron emission tomography using the radiotracer [(11)C]-PE2I in non-human primates. The cited study also incorporated post-mortem TH and DAT quantification, but the supplied evidence does not specify acquisition parameters, dosing, or analysis methods.
The evidence is limited to a single stated use case in MPTP-treated non-human primates. No details are provided on tracer kinetics, imaging protocol, quantification strategy, or validation beyond association with post-mortem TH and DAT measurements.
Validation
Cell-freeBacteriaMammalianMouseHumanTherapeuticIndep. Replication
Supporting Sources
Ranked Claims
Dopamine degeneration in the MPTP non-human primate model was assessed using in vivo PET with [(11)C]-PE2I and post-mortem TH and DAT quantification.
DA degeneration was assessed by in vivo PET ([(11)C]-PE2I) and post-mortem TH and DAT quantification.
Dopamine degeneration in the MPTP non-human primate model was assessed using in vivo PET with [(11)C]-PE2I and post-mortem TH and DAT quantification.
DA degeneration was assessed by in vivo PET ([(11)C]-PE2I) and post-mortem TH and DAT quantification.
Dopamine degeneration in the MPTP non-human primate model was assessed using in vivo PET with [(11)C]-PE2I and post-mortem TH and DAT quantification.
DA degeneration was assessed by in vivo PET ([(11)C]-PE2I) and post-mortem TH and DAT quantification.
Dopamine degeneration in the MPTP non-human primate model was assessed using in vivo PET with [(11)C]-PE2I and post-mortem TH and DAT quantification.
DA degeneration was assessed by in vivo PET ([(11)C]-PE2I) and post-mortem TH and DAT quantification.
Dopamine degeneration in the MPTP non-human primate model was assessed using in vivo PET with [(11)C]-PE2I and post-mortem TH and DAT quantification.
DA degeneration was assessed by in vivo PET ([(11)C]-PE2I) and post-mortem TH and DAT quantification.
Dopamine degeneration in the MPTP non-human primate model was assessed using in vivo PET with [(11)C]-PE2I and post-mortem TH and DAT quantification.
DA degeneration was assessed by in vivo PET ([(11)C]-PE2I) and post-mortem TH and DAT quantification.
Dopamine degeneration in the MPTP non-human primate model was assessed using in vivo PET with [(11)C]-PE2I and post-mortem TH and DAT quantification.
DA degeneration was assessed by in vivo PET ([(11)C]-PE2I) and post-mortem TH and DAT quantification.
Dopamine degeneration in the MPTP non-human primate model was assessed using in vivo PET with [(11)C]-PE2I and post-mortem TH and DAT quantification.
DA degeneration was assessed by in vivo PET ([(11)C]-PE2I) and post-mortem TH and DAT quantification.
Dopamine degeneration in the MPTP non-human primate model was assessed using in vivo PET with [(11)C]-PE2I and post-mortem TH and DAT quantification.
DA degeneration was assessed by in vivo PET ([(11)C]-PE2I) and post-mortem TH and DAT quantification.
Dopamine degeneration in the MPTP non-human primate model was assessed using in vivo PET with [(11)C]-PE2I and post-mortem TH and DAT quantification.
DA degeneration was assessed by in vivo PET ([(11)C]-PE2I) and post-mortem TH and DAT quantification.
Dopamine degeneration in the MPTP non-human primate model was assessed using in vivo PET with [(11)C]-PE2I and post-mortem TH and DAT quantification.
DA degeneration was assessed by in vivo PET ([(11)C]-PE2I) and post-mortem TH and DAT quantification.
Dopamine degeneration in the MPTP non-human primate model was assessed using in vivo PET with [(11)C]-PE2I and post-mortem TH and DAT quantification.
DA degeneration was assessed by in vivo PET ([(11)C]-PE2I) and post-mortem TH and DAT quantification.
Dopamine degeneration in the MPTP non-human primate model was assessed using in vivo PET with [(11)C]-PE2I and post-mortem TH and DAT quantification.
DA degeneration was assessed by in vivo PET ([(11)C]-PE2I) and post-mortem TH and DAT quantification.
Dopamine degeneration in the MPTP non-human primate model was assessed using in vivo PET with [(11)C]-PE2I and post-mortem TH and DAT quantification.
DA degeneration was assessed by in vivo PET ([(11)C]-PE2I) and post-mortem TH and DAT quantification.
Dopamine degeneration in the MPTP non-human primate model was assessed using in vivo PET with [(11)C]-PE2I and post-mortem TH and DAT quantification.
DA degeneration was assessed by in vivo PET ([(11)C]-PE2I) and post-mortem TH and DAT quantification.
Dopamine degeneration in the MPTP non-human primate model was assessed using in vivo PET with [(11)C]-PE2I and post-mortem TH and DAT quantification.
DA degeneration was assessed by in vivo PET ([(11)C]-PE2I) and post-mortem TH and DAT quantification.
Dopamine degeneration in the MPTP non-human primate model was assessed using in vivo PET with [(11)C]-PE2I and post-mortem TH and DAT quantification.
DA degeneration was assessed by in vivo PET ([(11)C]-PE2I) and post-mortem TH and DAT quantification.
Dopamine degeneration in the MPTP non-human primate model was assessed using in vivo PET with [(11)C]-PE2I and post-mortem TH and DAT quantification.
DA degeneration was assessed by in vivo PET ([(11)C]-PE2I) and post-mortem TH and DAT quantification.
Dopamine degeneration in the MPTP non-human primate model was assessed using in vivo PET with [(11)C]-PE2I and post-mortem TH and DAT quantification.
DA degeneration was assessed by in vivo PET ([(11)C]-PE2I) and post-mortem TH and DAT quantification.
Dopamine degeneration in the MPTP non-human primate model was assessed using in vivo PET with [(11)C]-PE2I and post-mortem TH and DAT quantification.
DA degeneration was assessed by in vivo PET ([(11)C]-PE2I) and post-mortem TH and DAT quantification.
Dopamine degeneration in the MPTP non-human primate model was assessed using in vivo PET with [(11)C]-PE2I and post-mortem TH and DAT quantification.
DA degeneration was assessed by in vivo PET ([(11)C]-PE2I) and post-mortem TH and DAT quantification.
Dopamine degeneration in the MPTP non-human primate model was assessed using in vivo PET with [(11)C]-PE2I and post-mortem TH and DAT quantification.
DA degeneration was assessed by in vivo PET ([(11)C]-PE2I) and post-mortem TH and DAT quantification.
Dopamine degeneration in the MPTP non-human primate model was assessed using in vivo PET with [(11)C]-PE2I and post-mortem TH and DAT quantification.
DA degeneration was assessed by in vivo PET ([(11)C]-PE2I) and post-mortem TH and DAT quantification.
Dopamine degeneration in the MPTP non-human primate model was assessed using in vivo PET with [(11)C]-PE2I and post-mortem TH and DAT quantification.
DA degeneration was assessed by in vivo PET ([(11)C]-PE2I) and post-mortem TH and DAT quantification.
Dopamine degeneration in the MPTP non-human primate model was assessed using in vivo PET with [(11)C]-PE2I and post-mortem TH and DAT quantification.
DA degeneration was assessed by in vivo PET ([(11)C]-PE2I) and post-mortem TH and DAT quantification.
Dopamine degeneration in the MPTP non-human primate model was assessed using in vivo PET with [(11)C]-PE2I and post-mortem TH and DAT quantification.
DA degeneration was assessed by in vivo PET ([(11)C]-PE2I) and post-mortem TH and DAT quantification.
Dopamine degeneration in the MPTP non-human primate model was assessed using in vivo PET with [(11)C]-PE2I and post-mortem TH and DAT quantification.
DA degeneration was assessed by in vivo PET ([(11)C]-PE2I) and post-mortem TH and DAT quantification.
Under constant light, dopamine-depleted non-human primates have severely disturbed or abolished locomotor rhythms, while controls retain free-running locomotor rest-wake and hormonal rhythms with stable phase relationships.
When the circadian system is challenged by exposure to constant light, controls retain locomotor rest-wake and hormonal rhythms that free-run with stable phase relationships whereas in the DA-depleted NHP, locomotor rhythms are severely disturbed or completely abolished.
Under constant light, dopamine-depleted non-human primates have severely disturbed or abolished locomotor rhythms, while controls retain free-running locomotor rest-wake and hormonal rhythms with stable phase relationships.
When the circadian system is challenged by exposure to constant light, controls retain locomotor rest-wake and hormonal rhythms that free-run with stable phase relationships whereas in the DA-depleted NHP, locomotor rhythms are severely disturbed or completely abolished.
Under constant light, dopamine-depleted non-human primates have severely disturbed or abolished locomotor rhythms, while controls retain free-running locomotor rest-wake and hormonal rhythms with stable phase relationships.
When the circadian system is challenged by exposure to constant light, controls retain locomotor rest-wake and hormonal rhythms that free-run with stable phase relationships whereas in the DA-depleted NHP, locomotor rhythms are severely disturbed or completely abolished.
Under constant light, dopamine-depleted non-human primates have severely disturbed or abolished locomotor rhythms, while controls retain free-running locomotor rest-wake and hormonal rhythms with stable phase relationships.
When the circadian system is challenged by exposure to constant light, controls retain locomotor rest-wake and hormonal rhythms that free-run with stable phase relationships whereas in the DA-depleted NHP, locomotor rhythms are severely disturbed or completely abolished.
Under constant light, dopamine-depleted non-human primates have severely disturbed or abolished locomotor rhythms, while controls retain free-running locomotor rest-wake and hormonal rhythms with stable phase relationships.
When the circadian system is challenged by exposure to constant light, controls retain locomotor rest-wake and hormonal rhythms that free-run with stable phase relationships whereas in the DA-depleted NHP, locomotor rhythms are severely disturbed or completely abolished.
Under constant light, dopamine-depleted non-human primates have severely disturbed or abolished locomotor rhythms, while controls retain free-running locomotor rest-wake and hormonal rhythms with stable phase relationships.
When the circadian system is challenged by exposure to constant light, controls retain locomotor rest-wake and hormonal rhythms that free-run with stable phase relationships whereas in the DA-depleted NHP, locomotor rhythms are severely disturbed or completely abolished.
Under constant light, dopamine-depleted non-human primates have severely disturbed or abolished locomotor rhythms, while controls retain free-running locomotor rest-wake and hormonal rhythms with stable phase relationships.
When the circadian system is challenged by exposure to constant light, controls retain locomotor rest-wake and hormonal rhythms that free-run with stable phase relationships whereas in the DA-depleted NHP, locomotor rhythms are severely disturbed or completely abolished.
Under constant light, dopamine-depleted non-human primates have severely disturbed or abolished locomotor rhythms, while controls retain free-running locomotor rest-wake and hormonal rhythms with stable phase relationships.
When the circadian system is challenged by exposure to constant light, controls retain locomotor rest-wake and hormonal rhythms that free-run with stable phase relationships whereas in the DA-depleted NHP, locomotor rhythms are severely disturbed or completely abolished.
Under constant light, dopamine-depleted non-human primates have severely disturbed or abolished locomotor rhythms, while controls retain free-running locomotor rest-wake and hormonal rhythms with stable phase relationships.
When the circadian system is challenged by exposure to constant light, controls retain locomotor rest-wake and hormonal rhythms that free-run with stable phase relationships whereas in the DA-depleted NHP, locomotor rhythms are severely disturbed or completely abolished.
Under constant light, dopamine-depleted non-human primates have severely disturbed or abolished locomotor rhythms, while controls retain free-running locomotor rest-wake and hormonal rhythms with stable phase relationships.
When the circadian system is challenged by exposure to constant light, controls retain locomotor rest-wake and hormonal rhythms that free-run with stable phase relationships whereas in the DA-depleted NHP, locomotor rhythms are severely disturbed or completely abolished.
Under constant light, dopamine-depleted non-human primates have severely disturbed or abolished locomotor rhythms, while controls retain free-running locomotor rest-wake and hormonal rhythms with stable phase relationships.
When the circadian system is challenged by exposure to constant light, controls retain locomotor rest-wake and hormonal rhythms that free-run with stable phase relationships whereas in the DA-depleted NHP, locomotor rhythms are severely disturbed or completely abolished.
Under constant light, dopamine-depleted non-human primates have severely disturbed or abolished locomotor rhythms, while controls retain free-running locomotor rest-wake and hormonal rhythms with stable phase relationships.
When the circadian system is challenged by exposure to constant light, controls retain locomotor rest-wake and hormonal rhythms that free-run with stable phase relationships whereas in the DA-depleted NHP, locomotor rhythms are severely disturbed or completely abolished.
Under constant light, dopamine-depleted non-human primates have severely disturbed or abolished locomotor rhythms, while controls retain free-running locomotor rest-wake and hormonal rhythms with stable phase relationships.
When the circadian system is challenged by exposure to constant light, controls retain locomotor rest-wake and hormonal rhythms that free-run with stable phase relationships whereas in the DA-depleted NHP, locomotor rhythms are severely disturbed or completely abolished.
Under constant light, dopamine-depleted non-human primates have severely disturbed or abolished locomotor rhythms, while controls retain free-running locomotor rest-wake and hormonal rhythms with stable phase relationships.
When the circadian system is challenged by exposure to constant light, controls retain locomotor rest-wake and hormonal rhythms that free-run with stable phase relationships whereas in the DA-depleted NHP, locomotor rhythms are severely disturbed or completely abolished.
Under constant light, dopamine-depleted non-human primates have severely disturbed or abolished locomotor rhythms, while controls retain free-running locomotor rest-wake and hormonal rhythms with stable phase relationships.
When the circadian system is challenged by exposure to constant light, controls retain locomotor rest-wake and hormonal rhythms that free-run with stable phase relationships whereas in the DA-depleted NHP, locomotor rhythms are severely disturbed or completely abolished.
Under constant light, dopamine-depleted non-human primates have severely disturbed or abolished locomotor rhythms, while controls retain free-running locomotor rest-wake and hormonal rhythms with stable phase relationships.
When the circadian system is challenged by exposure to constant light, controls retain locomotor rest-wake and hormonal rhythms that free-run with stable phase relationships whereas in the DA-depleted NHP, locomotor rhythms are severely disturbed or completely abolished.
Under constant light, dopamine-depleted non-human primates have severely disturbed or abolished locomotor rhythms, while controls retain free-running locomotor rest-wake and hormonal rhythms with stable phase relationships.
When the circadian system is challenged by exposure to constant light, controls retain locomotor rest-wake and hormonal rhythms that free-run with stable phase relationships whereas in the DA-depleted NHP, locomotor rhythms are severely disturbed or completely abolished.
Under constant light, dopamine-depleted non-human primates have severely disturbed or abolished locomotor rhythms, while controls retain free-running locomotor rest-wake and hormonal rhythms with stable phase relationships.
When the circadian system is challenged by exposure to constant light, controls retain locomotor rest-wake and hormonal rhythms that free-run with stable phase relationships whereas in the DA-depleted NHP, locomotor rhythms are severely disturbed or completely abolished.
Under constant light, dopamine-depleted non-human primates have severely disturbed or abolished locomotor rhythms, while controls retain free-running locomotor rest-wake and hormonal rhythms with stable phase relationships.
When the circadian system is challenged by exposure to constant light, controls retain locomotor rest-wake and hormonal rhythms that free-run with stable phase relationships whereas in the DA-depleted NHP, locomotor rhythms are severely disturbed or completely abolished.
Under constant light, dopamine-depleted non-human primates have severely disturbed or abolished locomotor rhythms, while controls retain free-running locomotor rest-wake and hormonal rhythms with stable phase relationships.
When the circadian system is challenged by exposure to constant light, controls retain locomotor rest-wake and hormonal rhythms that free-run with stable phase relationships whereas in the DA-depleted NHP, locomotor rhythms are severely disturbed or completely abolished.
Hormonal rhythm amplitude and phase relations remain unaltered in dopamine-depleted non-human primates despite locomotor rhythm disruption under constant light.
The amplitude and phase relations of hormonal rhythms nevertheless remain unaltered.
Hormonal rhythm amplitude and phase relations remain unaltered in dopamine-depleted non-human primates despite locomotor rhythm disruption under constant light.
The amplitude and phase relations of hormonal rhythms nevertheless remain unaltered.
Hormonal rhythm amplitude and phase relations remain unaltered in dopamine-depleted non-human primates despite locomotor rhythm disruption under constant light.
The amplitude and phase relations of hormonal rhythms nevertheless remain unaltered.
Hormonal rhythm amplitude and phase relations remain unaltered in dopamine-depleted non-human primates despite locomotor rhythm disruption under constant light.
The amplitude and phase relations of hormonal rhythms nevertheless remain unaltered.
Hormonal rhythm amplitude and phase relations remain unaltered in dopamine-depleted non-human primates despite locomotor rhythm disruption under constant light.
The amplitude and phase relations of hormonal rhythms nevertheless remain unaltered.
Hormonal rhythm amplitude and phase relations remain unaltered in dopamine-depleted non-human primates despite locomotor rhythm disruption under constant light.
The amplitude and phase relations of hormonal rhythms nevertheless remain unaltered.
Hormonal rhythm amplitude and phase relations remain unaltered in dopamine-depleted non-human primates despite locomotor rhythm disruption under constant light.
The amplitude and phase relations of hormonal rhythms nevertheless remain unaltered.
Hormonal rhythm amplitude and phase relations remain unaltered in dopamine-depleted non-human primates despite locomotor rhythm disruption under constant light.
The amplitude and phase relations of hormonal rhythms nevertheless remain unaltered.
Hormonal rhythm amplitude and phase relations remain unaltered in dopamine-depleted non-human primates despite locomotor rhythm disruption under constant light.
The amplitude and phase relations of hormonal rhythms nevertheless remain unaltered.
Hormonal rhythm amplitude and phase relations remain unaltered in dopamine-depleted non-human primates despite locomotor rhythm disruption under constant light.
The amplitude and phase relations of hormonal rhythms nevertheless remain unaltered.
Hormonal rhythm amplitude and phase relations remain unaltered in dopamine-depleted non-human primates despite locomotor rhythm disruption under constant light.
The amplitude and phase relations of hormonal rhythms nevertheless remain unaltered.
Hormonal rhythm amplitude and phase relations remain unaltered in dopamine-depleted non-human primates despite locomotor rhythm disruption under constant light.
The amplitude and phase relations of hormonal rhythms nevertheless remain unaltered.
Hormonal rhythm amplitude and phase relations remain unaltered in dopamine-depleted non-human primates despite locomotor rhythm disruption under constant light.
The amplitude and phase relations of hormonal rhythms nevertheless remain unaltered.
Hormonal rhythm amplitude and phase relations remain unaltered in dopamine-depleted non-human primates despite locomotor rhythm disruption under constant light.
The amplitude and phase relations of hormonal rhythms nevertheless remain unaltered.
Hormonal rhythm amplitude and phase relations remain unaltered in dopamine-depleted non-human primates despite locomotor rhythm disruption under constant light.
The amplitude and phase relations of hormonal rhythms nevertheless remain unaltered.
Hormonal rhythm amplitude and phase relations remain unaltered in dopamine-depleted non-human primates despite locomotor rhythm disruption under constant light.
The amplitude and phase relations of hormonal rhythms nevertheless remain unaltered.
Hormonal rhythm amplitude and phase relations remain unaltered in dopamine-depleted non-human primates despite locomotor rhythm disruption under constant light.
The amplitude and phase relations of hormonal rhythms nevertheless remain unaltered.
Hormonal rhythm amplitude and phase relations remain unaltered in dopamine-depleted non-human primates despite locomotor rhythm disruption under constant light.
The amplitude and phase relations of hormonal rhythms nevertheless remain unaltered.
Hormonal rhythm amplitude and phase relations remain unaltered in dopamine-depleted non-human primates despite locomotor rhythm disruption under constant light.
The amplitude and phase relations of hormonal rhythms nevertheless remain unaltered.
Hormonal rhythm amplitude and phase relations remain unaltered in dopamine-depleted non-human primates despite locomotor rhythm disruption under constant light.
The amplitude and phase relations of hormonal rhythms nevertheless remain unaltered.
Following dopamine lesion, the central clock in the SCN may remain intact, but without environmental timing cues it may be unable to drive downstream striatal clock gene and dopaminergic processes controlling locomotor output.
These results suggest that following DA lesion, the central clock in the SCN remains intact but, in the absence of environmental timing cues, is unable to drive downstream rhythmic processes of striatal clock gene and dopaminergic functions that control locomotor output.
Following dopamine lesion, the central clock in the SCN may remain intact, but without environmental timing cues it may be unable to drive downstream striatal clock gene and dopaminergic processes controlling locomotor output.
These results suggest that following DA lesion, the central clock in the SCN remains intact but, in the absence of environmental timing cues, is unable to drive downstream rhythmic processes of striatal clock gene and dopaminergic functions that control locomotor output.
Following dopamine lesion, the central clock in the SCN may remain intact, but without environmental timing cues it may be unable to drive downstream striatal clock gene and dopaminergic processes controlling locomotor output.
These results suggest that following DA lesion, the central clock in the SCN remains intact but, in the absence of environmental timing cues, is unable to drive downstream rhythmic processes of striatal clock gene and dopaminergic functions that control locomotor output.
Following dopamine lesion, the central clock in the SCN may remain intact, but without environmental timing cues it may be unable to drive downstream striatal clock gene and dopaminergic processes controlling locomotor output.
These results suggest that following DA lesion, the central clock in the SCN remains intact but, in the absence of environmental timing cues, is unable to drive downstream rhythmic processes of striatal clock gene and dopaminergic functions that control locomotor output.
Following dopamine lesion, the central clock in the SCN may remain intact, but without environmental timing cues it may be unable to drive downstream striatal clock gene and dopaminergic processes controlling locomotor output.
These results suggest that following DA lesion, the central clock in the SCN remains intact but, in the absence of environmental timing cues, is unable to drive downstream rhythmic processes of striatal clock gene and dopaminergic functions that control locomotor output.
Following dopamine lesion, the central clock in the SCN may remain intact, but without environmental timing cues it may be unable to drive downstream striatal clock gene and dopaminergic processes controlling locomotor output.
These results suggest that following DA lesion, the central clock in the SCN remains intact but, in the absence of environmental timing cues, is unable to drive downstream rhythmic processes of striatal clock gene and dopaminergic functions that control locomotor output.
Following dopamine lesion, the central clock in the SCN may remain intact, but without environmental timing cues it may be unable to drive downstream striatal clock gene and dopaminergic processes controlling locomotor output.
These results suggest that following DA lesion, the central clock in the SCN remains intact but, in the absence of environmental timing cues, is unable to drive downstream rhythmic processes of striatal clock gene and dopaminergic functions that control locomotor output.
Following dopamine lesion, the central clock in the SCN may remain intact, but without environmental timing cues it may be unable to drive downstream striatal clock gene and dopaminergic processes controlling locomotor output.
These results suggest that following DA lesion, the central clock in the SCN remains intact but, in the absence of environmental timing cues, is unable to drive downstream rhythmic processes of striatal clock gene and dopaminergic functions that control locomotor output.
Following dopamine lesion, the central clock in the SCN may remain intact, but without environmental timing cues it may be unable to drive downstream striatal clock gene and dopaminergic processes controlling locomotor output.
These results suggest that following DA lesion, the central clock in the SCN remains intact but, in the absence of environmental timing cues, is unable to drive downstream rhythmic processes of striatal clock gene and dopaminergic functions that control locomotor output.
Following dopamine lesion, the central clock in the SCN may remain intact, but without environmental timing cues it may be unable to drive downstream striatal clock gene and dopaminergic processes controlling locomotor output.
These results suggest that following DA lesion, the central clock in the SCN remains intact but, in the absence of environmental timing cues, is unable to drive downstream rhythmic processes of striatal clock gene and dopaminergic functions that control locomotor output.
Following dopamine lesion, the central clock in the SCN may remain intact, but without environmental timing cues it may be unable to drive downstream striatal clock gene and dopaminergic processes controlling locomotor output.
These results suggest that following DA lesion, the central clock in the SCN remains intact but, in the absence of environmental timing cues, is unable to drive downstream rhythmic processes of striatal clock gene and dopaminergic functions that control locomotor output.
Following dopamine lesion, the central clock in the SCN may remain intact, but without environmental timing cues it may be unable to drive downstream striatal clock gene and dopaminergic processes controlling locomotor output.
These results suggest that following DA lesion, the central clock in the SCN remains intact but, in the absence of environmental timing cues, is unable to drive downstream rhythmic processes of striatal clock gene and dopaminergic functions that control locomotor output.
Following dopamine lesion, the central clock in the SCN may remain intact, but without environmental timing cues it may be unable to drive downstream striatal clock gene and dopaminergic processes controlling locomotor output.
These results suggest that following DA lesion, the central clock in the SCN remains intact but, in the absence of environmental timing cues, is unable to drive downstream rhythmic processes of striatal clock gene and dopaminergic functions that control locomotor output.
Following dopamine lesion, the central clock in the SCN may remain intact, but without environmental timing cues it may be unable to drive downstream striatal clock gene and dopaminergic processes controlling locomotor output.
These results suggest that following DA lesion, the central clock in the SCN remains intact but, in the absence of environmental timing cues, is unable to drive downstream rhythmic processes of striatal clock gene and dopaminergic functions that control locomotor output.
Following dopamine lesion, the central clock in the SCN may remain intact, but without environmental timing cues it may be unable to drive downstream striatal clock gene and dopaminergic processes controlling locomotor output.
These results suggest that following DA lesion, the central clock in the SCN remains intact but, in the absence of environmental timing cues, is unable to drive downstream rhythmic processes of striatal clock gene and dopaminergic functions that control locomotor output.
Following dopamine lesion, the central clock in the SCN may remain intact, but without environmental timing cues it may be unable to drive downstream striatal clock gene and dopaminergic processes controlling locomotor output.
These results suggest that following DA lesion, the central clock in the SCN remains intact but, in the absence of environmental timing cues, is unable to drive downstream rhythmic processes of striatal clock gene and dopaminergic functions that control locomotor output.
Following dopamine lesion, the central clock in the SCN may remain intact, but without environmental timing cues it may be unable to drive downstream striatal clock gene and dopaminergic processes controlling locomotor output.
These results suggest that following DA lesion, the central clock in the SCN remains intact but, in the absence of environmental timing cues, is unable to drive downstream rhythmic processes of striatal clock gene and dopaminergic functions that control locomotor output.
Following dopamine lesion, the central clock in the SCN may remain intact, but without environmental timing cues it may be unable to drive downstream striatal clock gene and dopaminergic processes controlling locomotor output.
These results suggest that following DA lesion, the central clock in the SCN remains intact but, in the absence of environmental timing cues, is unable to drive downstream rhythmic processes of striatal clock gene and dopaminergic functions that control locomotor output.
Following dopamine lesion, the central clock in the SCN may remain intact, but without environmental timing cues it may be unable to drive downstream striatal clock gene and dopaminergic processes controlling locomotor output.
These results suggest that following DA lesion, the central clock in the SCN remains intact but, in the absence of environmental timing cues, is unable to drive downstream rhythmic processes of striatal clock gene and dopaminergic functions that control locomotor output.
Following dopamine lesion, the central clock in the SCN may remain intact, but without environmental timing cues it may be unable to drive downstream striatal clock gene and dopaminergic processes controlling locomotor output.
These results suggest that following DA lesion, the central clock in the SCN remains intact but, in the absence of environmental timing cues, is unable to drive downstream rhythmic processes of striatal clock gene and dopaminergic functions that control locomotor output.
In a light-dark cycle, MPTP-treated dopamine-depleted non-human primates retain rest-wake locomotor rhythms but show reduced amplitude, decreased stability, and increased fragmentation relative to controls.
In a light∶dark cycle, control and MPTP-treated NHP both exhibit rest-wake locomotor rhythms, although DA-depleted NHP show reduced amplitude, decreased stability and increased fragmentation.
In a light-dark cycle, MPTP-treated dopamine-depleted non-human primates retain rest-wake locomotor rhythms but show reduced amplitude, decreased stability, and increased fragmentation relative to controls.
In a light∶dark cycle, control and MPTP-treated NHP both exhibit rest-wake locomotor rhythms, although DA-depleted NHP show reduced amplitude, decreased stability and increased fragmentation.
In a light-dark cycle, MPTP-treated dopamine-depleted non-human primates retain rest-wake locomotor rhythms but show reduced amplitude, decreased stability, and increased fragmentation relative to controls.
In a light∶dark cycle, control and MPTP-treated NHP both exhibit rest-wake locomotor rhythms, although DA-depleted NHP show reduced amplitude, decreased stability and increased fragmentation.
In a light-dark cycle, MPTP-treated dopamine-depleted non-human primates retain rest-wake locomotor rhythms but show reduced amplitude, decreased stability, and increased fragmentation relative to controls.
In a light∶dark cycle, control and MPTP-treated NHP both exhibit rest-wake locomotor rhythms, although DA-depleted NHP show reduced amplitude, decreased stability and increased fragmentation.
In a light-dark cycle, MPTP-treated dopamine-depleted non-human primates retain rest-wake locomotor rhythms but show reduced amplitude, decreased stability, and increased fragmentation relative to controls.
In a light∶dark cycle, control and MPTP-treated NHP both exhibit rest-wake locomotor rhythms, although DA-depleted NHP show reduced amplitude, decreased stability and increased fragmentation.
In a light-dark cycle, MPTP-treated dopamine-depleted non-human primates retain rest-wake locomotor rhythms but show reduced amplitude, decreased stability, and increased fragmentation relative to controls.
In a light∶dark cycle, control and MPTP-treated NHP both exhibit rest-wake locomotor rhythms, although DA-depleted NHP show reduced amplitude, decreased stability and increased fragmentation.
In a light-dark cycle, MPTP-treated dopamine-depleted non-human primates retain rest-wake locomotor rhythms but show reduced amplitude, decreased stability, and increased fragmentation relative to controls.
In a light∶dark cycle, control and MPTP-treated NHP both exhibit rest-wake locomotor rhythms, although DA-depleted NHP show reduced amplitude, decreased stability and increased fragmentation.
In a light-dark cycle, MPTP-treated dopamine-depleted non-human primates retain rest-wake locomotor rhythms but show reduced amplitude, decreased stability, and increased fragmentation relative to controls.
In a light∶dark cycle, control and MPTP-treated NHP both exhibit rest-wake locomotor rhythms, although DA-depleted NHP show reduced amplitude, decreased stability and increased fragmentation.
In a light-dark cycle, MPTP-treated dopamine-depleted non-human primates retain rest-wake locomotor rhythms but show reduced amplitude, decreased stability, and increased fragmentation relative to controls.
In a light∶dark cycle, control and MPTP-treated NHP both exhibit rest-wake locomotor rhythms, although DA-depleted NHP show reduced amplitude, decreased stability and increased fragmentation.
In a light-dark cycle, MPTP-treated dopamine-depleted non-human primates retain rest-wake locomotor rhythms but show reduced amplitude, decreased stability, and increased fragmentation relative to controls.
In a light∶dark cycle, control and MPTP-treated NHP both exhibit rest-wake locomotor rhythms, although DA-depleted NHP show reduced amplitude, decreased stability and increased fragmentation.
In a light-dark cycle, MPTP-treated dopamine-depleted non-human primates retain rest-wake locomotor rhythms but show reduced amplitude, decreased stability, and increased fragmentation relative to controls.
In a light∶dark cycle, control and MPTP-treated NHP both exhibit rest-wake locomotor rhythms, although DA-depleted NHP show reduced amplitude, decreased stability and increased fragmentation.
In a light-dark cycle, MPTP-treated dopamine-depleted non-human primates retain rest-wake locomotor rhythms but show reduced amplitude, decreased stability, and increased fragmentation relative to controls.
In a light∶dark cycle, control and MPTP-treated NHP both exhibit rest-wake locomotor rhythms, although DA-depleted NHP show reduced amplitude, decreased stability and increased fragmentation.
In a light-dark cycle, MPTP-treated dopamine-depleted non-human primates retain rest-wake locomotor rhythms but show reduced amplitude, decreased stability, and increased fragmentation relative to controls.
In a light∶dark cycle, control and MPTP-treated NHP both exhibit rest-wake locomotor rhythms, although DA-depleted NHP show reduced amplitude, decreased stability and increased fragmentation.
In a light-dark cycle, MPTP-treated dopamine-depleted non-human primates retain rest-wake locomotor rhythms but show reduced amplitude, decreased stability, and increased fragmentation relative to controls.
In a light∶dark cycle, control and MPTP-treated NHP both exhibit rest-wake locomotor rhythms, although DA-depleted NHP show reduced amplitude, decreased stability and increased fragmentation.
In a light-dark cycle, MPTP-treated dopamine-depleted non-human primates retain rest-wake locomotor rhythms but show reduced amplitude, decreased stability, and increased fragmentation relative to controls.
In a light∶dark cycle, control and MPTP-treated NHP both exhibit rest-wake locomotor rhythms, although DA-depleted NHP show reduced amplitude, decreased stability and increased fragmentation.
In a light-dark cycle, MPTP-treated dopamine-depleted non-human primates retain rest-wake locomotor rhythms but show reduced amplitude, decreased stability, and increased fragmentation relative to controls.
In a light∶dark cycle, control and MPTP-treated NHP both exhibit rest-wake locomotor rhythms, although DA-depleted NHP show reduced amplitude, decreased stability and increased fragmentation.
In a light-dark cycle, MPTP-treated dopamine-depleted non-human primates retain rest-wake locomotor rhythms but show reduced amplitude, decreased stability, and increased fragmentation relative to controls.
In a light∶dark cycle, control and MPTP-treated NHP both exhibit rest-wake locomotor rhythms, although DA-depleted NHP show reduced amplitude, decreased stability and increased fragmentation.
In a light-dark cycle, MPTP-treated dopamine-depleted non-human primates retain rest-wake locomotor rhythms but show reduced amplitude, decreased stability, and increased fragmentation relative to controls.
In a light∶dark cycle, control and MPTP-treated NHP both exhibit rest-wake locomotor rhythms, although DA-depleted NHP show reduced amplitude, decreased stability and increased fragmentation.
In a light-dark cycle, MPTP-treated dopamine-depleted non-human primates retain rest-wake locomotor rhythms but show reduced amplitude, decreased stability, and increased fragmentation relative to controls.
In a light∶dark cycle, control and MPTP-treated NHP both exhibit rest-wake locomotor rhythms, although DA-depleted NHP show reduced amplitude, decreased stability and increased fragmentation.
In a light-dark cycle, MPTP-treated dopamine-depleted non-human primates retain rest-wake locomotor rhythms but show reduced amplitude, decreased stability, and increased fragmentation relative to controls.
In a light∶dark cycle, control and MPTP-treated NHP both exhibit rest-wake locomotor rhythms, although DA-depleted NHP show reduced amplitude, decreased stability and increased fragmentation.
Approval Evidence
1 source1 linked approval claimfirst-pass slug in-vivo-pet-11-c-pe2i
DA degeneration was assessed by in vivo PET ([(11)C]-PE2I) and post-mortem TH and DAT quantification.
Source:
assay usagesupports
Dopamine degeneration in the MPTP non-human primate model was assessed using in vivo PET with [(11)C]-PE2I and post-mortem TH and DAT quantification.
DA degeneration was assessed by in vivo PET ([(11)C]-PE2I) and post-mortem TH and DAT quantification.
Source:
Comparisons
Source-backed strengths
The method was used in vivo and paired with post-mortem tyrosine hydroxylase and dopamine transporter quantification, supporting its role in a cross-validated assessment workflow. The supplied evidence does not report sensitivity, specificity, spatial resolution, or longitudinal performance.
Compared with Field-domain rapid-scan EPR at 240 GHz
in vivo PET ([(11)C]-PE2I) and Field-domain rapid-scan EPR at 240 GHz address a similar problem space.
Shared frame: same top-level item type
Compared with fluorescence line narrowing
in vivo PET ([(11)C]-PE2I) and fluorescence line narrowing address a similar problem space.
Shared frame: same top-level item type
Compared with native green gel system
in vivo PET ([(11)C]-PE2I) and native green gel system address a similar problem space.
Shared frame: same top-level item type
Strengths here: looks easier to implement in practice.
Ranked Citations
- 1.