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PORTLAND, OR—In patients with idiopathic REM sleep behavior disorder, microglial activation is increased in the substantia nigra, compared with controls, and microglial activation correlates with putamenal dopaminergic dysfunction, according to research presented at the Fourth World Parkinson Congress. These findings suggest that “anti-inflammatory agents could possibly delay progression to a manifest synucleinopathy in subjects with idiopathic REM sleep behavior disorder,” researchers said.
Longitudinal studies have found that patients with idiopathic REM sleep behavior disorder have an increased risk of Parkinson’s disease and related Lewy body disorders. “This implies that, in idiopathic REM sleep behavior disorder, the underlying pathology of developing neurodegenerative disorders can be investigated years prior to the development of manifest symptoms,” said Morten Gersel Stokholm, MD, a researcher in the Department of Clinical Medicine at Aarhus University and the Department of Nuclear Medicine & PET-Centre at Aarhus University Hospital, Denmark, and his research colleagues. 
Chronic activation of microglial cells may have a detrimental effect on neurons and contribute to the development of neurodegenerative disorders. Studies have found that uptake of an in vivo marker of microglial activation, 11C-PK11195, is increased in Parkinson’s disease and other neurodegenerative disorders.
To investigate the in vivo occurrence of neuroinflammation in the brains of patients with idiopathic REM sleep behavior disorder and neuroinflammation’s temporal relationship with striatal dopamine dysfunction, Dr. Stokholm and colleagues conducted a multitracer PET study of patients with idiopathic REM sleep behavior disorder.
The investigators enrolled 15 patients with polysomnography-confirmed idiopathic REM sleep behavior disorder at Aarhus University Hospital and Hospital Clínic de Barcelona. They also enrolled 19 matched controls. Participants underwent two PET scans with 18F-DOPA and 11C- PK11195 and a structural T1 MRI scan. Parametric images of specific tracer uptake (ie, F-dopa Ki-values and PK11195 binding potential) were constructed at voxel level using Patlak graphical analysis and a supervised cluster-analysis with compartmental modeling, respectively. A region of interest analysis was performed on a priori defined regions.
Compared with controls, patients with idiopathic REM sleep behavior disorder showed significantly reduced 18F-DOPA tracer uptake in the substantia nigra. Patients with higher substantia nigra11C-PK11195 binding also had increased binding in the ipsilateral putamen. Patients with more severe reductions in putaminal 18F-DOPA uptake had significantly higher 11C-PK11195 binding in the putamen and substantia nigra.
—Jake Remaly
PORTLAND, OR—In patients with idiopathic REM sleep behavior disorder, microglial activation is increased in the substantia nigra, compared with controls, and microglial activation correlates with putamenal dopaminergic dysfunction, according to research presented at the Fourth World Parkinson Congress. These findings suggest that “anti-inflammatory agents could possibly delay progression to a manifest synucleinopathy in subjects with idiopathic REM sleep behavior disorder,” researchers said.
Longitudinal studies have found that patients with idiopathic REM sleep behavior disorder have an increased risk of Parkinson’s disease and related Lewy body disorders. “This implies that, in idiopathic REM sleep behavior disorder, the underlying pathology of developing neurodegenerative disorders can be investigated years prior to the development of manifest symptoms,” said Morten Gersel Stokholm, MD, a researcher in the Department of Clinical Medicine at Aarhus University and the Department of Nuclear Medicine & PET-Centre at Aarhus University Hospital, Denmark, and his research colleagues.
Chronic activation of microglial cells may have a detrimental effect on neurons and contribute to the development of neurodegenerative disorders. Studies have found that uptake of an in vivo marker of microglial activation, 11C-PK11195, is increased in Parkinson’s disease and other neurodegenerative disorders.
To investigate the in vivo occurrence of neuroinflammation in the brains of patients with idiopathic REM sleep behavior disorder and neuroinflammation’s temporal relationship with striatal dopamine dysfunction, Dr. Stokholm and colleagues conducted a multitracer PET study of patients with idiopathic REM sleep behavior disorder.
The investigators enrolled 15 patients with polysomnography-confirmed idiopathic REM sleep behavior disorder at Aarhus University Hospital and Hospital Clínic de Barcelona. They also enrolled 19 matched controls. Participants underwent two PET scans with 18F-DOPA and 11C- PK11195 and a structural T1 MRI scan. Parametric images of specific tracer uptake (ie, F-dopa Ki-values and PK11195 binding potential) were constructed at voxel level using Patlak graphical analysis and a supervised cluster-analysis with compartmental modeling, respectively. A region of interest analysis was performed on a priori defined regions.
Compared with controls, patients with idiopathic REM sleep behavior disorder showed significantly reduced 18F-DOPA tracer uptake in the substantia nigra. Patients with higher substantia nigra11C-PK11195 binding also had increased binding in the ipsilateral putamen. Patients with more severe reductions in putaminal 18F-DOPA uptake had significantly higher 11C-PK11195 binding in the putamen and substantia nigra.
—Jake Remaly
PORTLAND, OR—In patients with idiopathic REM sleep behavior disorder, microglial activation is increased in the substantia nigra, compared with controls, and microglial activation correlates with putamenal dopaminergic dysfunction, according to research presented at the Fourth World Parkinson Congress. These findings suggest that “anti-inflammatory agents could possibly delay progression to a manifest synucleinopathy in subjects with idiopathic REM sleep behavior disorder,” researchers said.
Longitudinal studies have found that patients with idiopathic REM sleep behavior disorder have an increased risk of Parkinson’s disease and related Lewy body disorders. “This implies that, in idiopathic REM sleep behavior disorder, the underlying pathology of developing neurodegenerative disorders can be investigated years prior to the development of manifest symptoms,” said Morten Gersel Stokholm, MD, a researcher in the Department of Clinical Medicine at Aarhus University and the Department of Nuclear Medicine & PET-Centre at Aarhus University Hospital, Denmark, and his research colleagues.
Chronic activation of microglial cells may have a detrimental effect on neurons and contribute to the development of neurodegenerative disorders. Studies have found that uptake of an in vivo marker of microglial activation, 11C-PK11195, is increased in Parkinson’s disease and other neurodegenerative disorders.
To investigate the in vivo occurrence of neuroinflammation in the brains of patients with idiopathic REM sleep behavior disorder and neuroinflammation’s temporal relationship with striatal dopamine dysfunction, Dr. Stokholm and colleagues conducted a multitracer PET study of patients with idiopathic REM sleep behavior disorder.
The investigators enrolled 15 patients with polysomnography-confirmed idiopathic REM sleep behavior disorder at Aarhus University Hospital and Hospital Clínic de Barcelona. They also enrolled 19 matched controls. Participants underwent two PET scans with 18F-DOPA and 11C- PK11195 and a structural T1 MRI scan. Parametric images of specific tracer uptake (ie, F-dopa Ki-values and PK11195 binding potential) were constructed at voxel level using Patlak graphical analysis and a supervised cluster-analysis with compartmental modeling, respectively. A region of interest analysis was performed on a priori defined regions.
Compared with controls, patients with idiopathic REM sleep behavior disorder showed significantly reduced 18F-DOPA tracer uptake in the substantia nigra. Patients with higher substantia nigra11C-PK11195 binding also had increased binding in the ipsilateral putamen. Patients with more severe reductions in putaminal 18F-DOPA uptake had significantly higher 11C-PK11195 binding in the putamen and substantia nigra.
—Jake Remaly