In vivo detection of neuropathologic changes in presymptomatic MAPT mutation carriers: A PET and MRI study
Microglial activation and disrupted neurotransmissions may herald symptomatic manifestations in neurodegenerative tauopathies. We investigated microglial activation with [ 11C]DAA1106 positron emission tomography (PET), striatal dopaminergic function with l-[β- 11C]dopa PET, acetylcholinesterase (AC...
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| Published in | Parkinsonism & related disorders Vol. 16; no. 6; pp. 404 - 408 |
|---|---|
| Main Authors | , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
England
Elsevier Ltd
01.07.2010
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| Subjects | |
| Online Access | Get full text |
| ISSN | 1353-8020 1873-5126 1873-5126 |
| DOI | 10.1016/j.parkreldis.2010.04.004 |
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| Abstract | Microglial activation and disrupted neurotransmissions may herald symptomatic manifestations in neurodegenerative tauopathies.
We investigated microglial activation with [
11C]DAA1106 positron emission tomography (PET), striatal dopaminergic function with
l-[β-
11C]dopa PET, acetylcholinesterase (AChE) activity with [
11C]
N-methylpiperidin-4-yl acetate PET, and morphologic brain changes with MRI in three persons (aged 38–41 years) with frontotemporal dementia with parkinsonism linked to chromosome 17 (FTDP-17), who were presymptomatic gene carriers (PGCs) from an American kindred with pallidopontonigral degeneration. The results from these 3 PGCs were compared with [
11C]DAA1106 PET results from age-matched 9 healthy volunteers (HV), and with
l-[β-
11C]dopa and [
11C]MP4A PET results from 10 HV. Values considered significant were more than 2 SDs greater or less than the normal control mean, as the number of subjects was small for group comparisons.
Glial activities were increased in the frontal cortex of one PGC, the occipital cortex of two PGCs, and the posterior cingulate cortex of one PGC, although none of the PGCs showed overt glial activation in the brain. Only one of the PGCs showed reduced AChE activity in the temporo-parietal cortex. Three PGCs showed low dopamine synthesis rates in the putamen. Hippocampal atrophy was observed in two PGCs.
Hippocampal atrophy and striatal dopaminergic dysfunction may be early disease processes in the pathogenesis of FTDP-17. Neuroinflammation may also be an in vivo signature of tau pathology at a prodromal stage, although current PET techniques may not constantly reveal it as the earliest neuroimaging abnormality. |
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| AbstractList | Microglial activation and disrupted neurotransmissions may herald symptomatic manifestations in neurodegenerative tauopathies.BACKGROUNDMicroglial activation and disrupted neurotransmissions may herald symptomatic manifestations in neurodegenerative tauopathies.We investigated microglial activation with [(11)C]DAA1106 positron emission tomography (PET), striatal dopaminergic function with l-[beta-(11)C]dopa PET, acetylcholinesterase (AChE) activity with [(11)C]N-methylpiperidin-4-yl acetate PET, and morphologic brain changes with MRI in three persons (aged 38-41 years) with frontotemporal dementia with parkinsonism linked to chromosome 17 (FTDP-17), who were presymptomatic gene carriers (PGCs) from an American kindred with pallidopontonigral degeneration. The results from these 3 PGCs were compared with [(11)C]DAA1106 PET results from age-matched 9 healthy volunteers (HV), and with l-[beta-(11)C]dopa and [(11)C]MP4A PET results from 10 HV. Values considered significant were more than 2 SDs greater or less than the normal control mean, as the number of subjects was small for group comparisons.METHODSWe investigated microglial activation with [(11)C]DAA1106 positron emission tomography (PET), striatal dopaminergic function with l-[beta-(11)C]dopa PET, acetylcholinesterase (AChE) activity with [(11)C]N-methylpiperidin-4-yl acetate PET, and morphologic brain changes with MRI in three persons (aged 38-41 years) with frontotemporal dementia with parkinsonism linked to chromosome 17 (FTDP-17), who were presymptomatic gene carriers (PGCs) from an American kindred with pallidopontonigral degeneration. The results from these 3 PGCs were compared with [(11)C]DAA1106 PET results from age-matched 9 healthy volunteers (HV), and with l-[beta-(11)C]dopa and [(11)C]MP4A PET results from 10 HV. Values considered significant were more than 2 SDs greater or less than the normal control mean, as the number of subjects was small for group comparisons.Glial activities were increased in the frontal cortex of one PGC, the occipital cortex of two PGCs, and the posterior cingulate cortex of one PGC, although none of the PGCs showed overt glial activation in the brain. Only one of the PGCs showed reduced AChE activity in the temporo-parietal cortex. Three PGCs showed low dopamine synthesis rates in the putamen. Hippocampal atrophy was observed in two PGCs.RESULTSGlial activities were increased in the frontal cortex of one PGC, the occipital cortex of two PGCs, and the posterior cingulate cortex of one PGC, although none of the PGCs showed overt glial activation in the brain. Only one of the PGCs showed reduced AChE activity in the temporo-parietal cortex. Three PGCs showed low dopamine synthesis rates in the putamen. Hippocampal atrophy was observed in two PGCs.Hippocampal atrophy and striatal dopaminergic dysfunction may be early disease processes in the pathogenesis of FTDP-17. Neuroinflammation may also be an in vivo signature of tau pathology at a prodromal stage, although current PET techniques may not constantly reveal it as the earliest neuroimaging abnormality.CONCLUSIONSHippocampal atrophy and striatal dopaminergic dysfunction may be early disease processes in the pathogenesis of FTDP-17. Neuroinflammation may also be an in vivo signature of tau pathology at a prodromal stage, although current PET techniques may not constantly reveal it as the earliest neuroimaging abnormality. Abstract Background Microglial activation and disrupted neurotransmissions may herald symptomatic manifestations in neurodegenerative tauopathies. Methods We investigated microglial activation with [11 C]DAA1106 positron emission tomography (PET), striatal dopaminergic function with l -[β-11 C]dopa PET, acetylcholinesterase (AChE) activity with [11 C] N -methylpiperidin-4-yl acetate PET, and morphologic brain changes with MRI in three persons (aged 38–41 years) with frontotemporal dementia with parkinsonism linked to chromosome 17 (FTDP-17), who were presymptomatic gene carriers (PGCs) from an American kindred with pallidopontonigral degeneration. The results from these 3 PGCs were compared with [11 C]DAA1106 PET results from age-matched 9 healthy volunteers (HV), and with l -[β-11 C]dopa and [11 C]MP4A PET results from 10 HV. Values considered significant were more than 2 SDs greater or less than the normal control mean, as the number of subjects was small for group comparisons. Results Glial activities were increased in the frontal cortex of one PGC, the occipital cortex of two PGCs, and the posterior cingulate cortex of one PGC, although none of the PGCs showed overt glial activation in the brain. Only one of the PGCs showed reduced AChE activity in the temporo-parietal cortex. Three PGCs showed low dopamine synthesis rates in the putamen. Hippocampal atrophy was observed in two PGCs. Conclusions Hippocampal atrophy and striatal dopaminergic dysfunction may be early disease processes in the pathogenesis of FTDP-17. Neuroinflammation may also be an in vivo signature of tau pathology at a prodromal stage, although current PET techniques may not constantly reveal it as the earliest neuroimaging abnormality. Microglial activation and disrupted neurotransmissions may herald symptomatic manifestations in neurodegenerative tauopathies. We investigated microglial activation with [(11)C]DAA1106 positron emission tomography (PET), striatal dopaminergic function with l-[beta-(11)C]dopa PET, acetylcholinesterase (AChE) activity with [(11)C]N-methylpiperidin-4-yl acetate PET, and morphologic brain changes with MRI in three persons (aged 38-41 years) with frontotemporal dementia with parkinsonism linked to chromosome 17 (FTDP-17), who were presymptomatic gene carriers (PGCs) from an American kindred with pallidopontonigral degeneration. The results from these 3 PGCs were compared with [(11)C]DAA1106 PET results from age-matched 9 healthy volunteers (HV), and with l-[beta-(11)C]dopa and [(11)C]MP4A PET results from 10 HV. Values considered significant were more than 2 SDs greater or less than the normal control mean, as the number of subjects was small for group comparisons. Glial activities were increased in the frontal cortex of one PGC, the occipital cortex of two PGCs, and the posterior cingulate cortex of one PGC, although none of the PGCs showed overt glial activation in the brain. Only one of the PGCs showed reduced AChE activity in the temporo-parietal cortex. Three PGCs showed low dopamine synthesis rates in the putamen. Hippocampal atrophy was observed in two PGCs. Hippocampal atrophy and striatal dopaminergic dysfunction may be early disease processes in the pathogenesis of FTDP-17. Neuroinflammation may also be an in vivo signature of tau pathology at a prodromal stage, although current PET techniques may not constantly reveal it as the earliest neuroimaging abnormality. Microglial activation and disrupted neurotransmissions may herald symptomatic manifestations in neurodegenerative tauopathies. We investigated microglial activation with [ 11C]DAA1106 positron emission tomography (PET), striatal dopaminergic function with l-[β- 11C]dopa PET, acetylcholinesterase (AChE) activity with [ 11C] N-methylpiperidin-4-yl acetate PET, and morphologic brain changes with MRI in three persons (aged 38–41 years) with frontotemporal dementia with parkinsonism linked to chromosome 17 (FTDP-17), who were presymptomatic gene carriers (PGCs) from an American kindred with pallidopontonigral degeneration. The results from these 3 PGCs were compared with [ 11C]DAA1106 PET results from age-matched 9 healthy volunteers (HV), and with l-[β- 11C]dopa and [ 11C]MP4A PET results from 10 HV. Values considered significant were more than 2 SDs greater or less than the normal control mean, as the number of subjects was small for group comparisons. Glial activities were increased in the frontal cortex of one PGC, the occipital cortex of two PGCs, and the posterior cingulate cortex of one PGC, although none of the PGCs showed overt glial activation in the brain. Only one of the PGCs showed reduced AChE activity in the temporo-parietal cortex. Three PGCs showed low dopamine synthesis rates in the putamen. Hippocampal atrophy was observed in two PGCs. Hippocampal atrophy and striatal dopaminergic dysfunction may be early disease processes in the pathogenesis of FTDP-17. Neuroinflammation may also be an in vivo signature of tau pathology at a prodromal stage, although current PET techniques may not constantly reveal it as the earliest neuroimaging abnormality. Microglial activation and disrupted neurotransmissions may herald symptomatic manifestations in neurodegenerative tauopathies. Methods - We investigated microglial activation with [ super(11)C]DAA1106 positron emission tomography (PET), striatal dopaminergic function with l-[ beta - super(11)C]dopa PET, acetylcholinesterase (AChE) activity with [ super(11)C]N-methylpiperidin-4-yl acetate PET, and morphologic brain changes with MRI in three persons (aged 38-41 years) with frontotemporal dementia with parkinsonism linked to chromosome 17 (FTDP-17), who were presymptomatic gene carriers (PGCs) from an American kindred with pallidopontonigral degeneration. The results from these 3 PGCs were compared with [ super(11)C]DAA1106 PET results from age-matched 9 healthy volunteers (HV), and with l-[ beta - super(11)C]dopa and [ super(11)C]MP4A PET results from 10 HV. Values considered significant were more than 2 SDs greater or less than the normal control mean, as the number of subjects was small for group comparisons. Results - Glial activities were increased in the frontal cortex of one PGC, the occipital cortex of two PGCs, and the posterior cingulate cortex of one PGC, although none of the PGCs showed overt glial activation in the brain. Only one of the PGCs showed reduced AChE activity in the temporo-parietal cortex. Three PGCs showed low dopamine synthesis rates in the putamen. Hippocampal atrophy was observed in two PGCs. Conclusions - Hippocampal atrophy and striatal dopaminergic dysfunction may be early disease processes in the pathogenesis of FTDP-17. Neuroinflammation may also be an in vivo signature of tau pathology at a prodromal stage, although current PET techniques may not constantly reveal it as the earliest neuroimaging abnormality. |
| Author | Yasuno, Fumihiko Irie, Toshiaki Shimada, Hitoshi Higuchi, Makoto Fukushi, Kiyoshi Ito, Hiroshi Strongosky, Audrey J. Arakawa, Ryosuke Suhara, Tetsuya Miyoshi, Michie Wszolek, Zbigniew K. Shinotoh, Hitoshi Ikoma, Yoko |
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| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/20452812$$D View this record in MEDLINE/PubMed |
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| Keywords | AChE PBR Dopamine MRI PBBS k ref [ 11C]dopa PGC BP ND Microglia PPND Magnetic resonance imaging MP4A FTDP-17 Acetylcholine Positron emission tomography PET k 3 pallidopontonigral degeneration binding potential hydrolysis rate constant presymptomatic gene carrier peripheral benzodiazepine binding site frontotemporal dementia with parkinsonism linked to chromosome 17 acetylcholinesterase an index of dopamine synthesis [ 11C] N-methylpiperidin-4-yl acetate peripheral benzodiazepine receptor l-[β- 11C]dopa |
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| Snippet | Microglial activation and disrupted neurotransmissions may herald symptomatic manifestations in neurodegenerative tauopathies.
We investigated microglial... Abstract Background Microglial activation and disrupted neurotransmissions may herald symptomatic manifestations in neurodegenerative tauopathies. Methods We... Microglial activation and disrupted neurotransmissions may herald symptomatic manifestations in neurodegenerative tauopathies.BACKGROUNDMicroglial activation... Microglial activation and disrupted neurotransmissions may herald symptomatic manifestations in neurodegenerative tauopathies. Methods - We investigated... |
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| SubjectTerms | Acetylcholine Adult Brain - diagnostic imaging Brain - pathology Dopamine Frontotemporal Dementia - diagnostic imaging Frontotemporal Dementia - genetics Frontotemporal Dementia - pathology FTDP-17 Heterozygote Humans Image Interpretation, Computer-Assisted Magnetic Resonance Imaging Microglia Mutation Neurology Neuropsychological Tests Positron emission tomography tau Proteins - genetics |
| Title | In vivo detection of neuropathologic changes in presymptomatic MAPT mutation carriers: A PET and MRI study |
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