Relationship between neuromelanin and dopamine terminals within the Parkinson’s nigrostriatal system
Parkinson’s disease is characterized by the progressive loss of pigmented dopaminergic neurons in the substantia nigra and associated striatal deafferentation. Neuromelanin content is thought to reflect the loss of pigmented neurons, but available data characterizing its relationship with striatal d...
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| Published in | Brain (London, England : 1878) Vol. 142; no. 7; pp. 2023 - 2036 |
|---|---|
| Main Authors | , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
England
Oxford University Press
01.07.2019
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| Subjects | |
| Online Access | Get full text |
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| Abstract | Parkinson’s disease is characterized by the progressive loss of pigmented dopaminergic neurons in the substantia nigra and associated striatal deafferentation. Neuromelanin content is thought to reflect the loss of pigmented neurons, but available data characterizing its relationship with striatal dopaminergic integrity are not comprehensive or consistent, and predominantly involve heterogeneous samples. In this cross-sectional study, we used neuromelanin-sensitive MRI and the highly specific dopamine transporter PET radioligand, 11C-PE2I, to assess the association between neuromelanin-containing cell levels in the substantia nigra pars compacta and nigrostriatal terminal density in vivo, in 30 patients with bilateral Parkinson’s disease. Fifteen healthy control subjects also underwent neuromelanin-sensitive imaging. We used a novel approach taking into account the anatomical and functional subdivision of substantia nigra into dorsal and ventral tiers and striatal nuclei into pre- and post-commissural subregions, in accordance with previous animal and post-mortem studies, and consider the clinically asymmetric disease presentation. In vivo, Parkinson’s disease subjects displayed reduced neuromelanin levels in the ventral (−30 ± 28%) and dorsal tiers (−21 ± 24%) as compared to the control group [F(1,43) = 11.95, P = 0.001]. Within the Parkinson’s disease group, nigral pigmentation was lower in the ventral tier as compared to the dorsal tier [F(1,29) = 36.19, P < 0.001] and lower in the clinically-defined most affected side [F(1,29) = 4.85, P = 0.036]. Similarly, lower dopamine transporter density was observed in the ventral tier [F(1,29) = 76.39, P < 0.001] and clinically-defined most affected side [F(1,29) = 4.21, P = 0.049]. Despite similar patterns, regression analysis showed no significant association between nigral pigmentation and nigral dopamine transporter density. However, for the clinically-defined most affected side, significant relationships were observed between pigmentation of the ventral nigral tier with striatal dopamine transporter binding in pre-commissural and post-commissural striatal subregions known to receive nigrostriatal projections from this tier, while the dorsal tier correlated with striatal projection sites in the pre-commissural striatum (P < 0.05, Benjamini-Hochberg corrected). In contrast, there were no statistically significant relationships between these two measures in the clinically-defined least affected side. These findings provide important insights into the topography of nigrostriatal neurodegeneration in Parkinson’s disease, indicating that the characteristics of disease progression may fundamentally differ across hemispheres and support post-mortem data showing asynchrony in the loss of neuromelanin-containing versus tyrosine hydroxylase positive nigral cells. |
|---|---|
| AbstractList | Striatal dopamine transporter density and nigral neuromelanin content are imaging biomarkers of nigrostriatal denervation and disease progression in Parkinson’s disease. Using neuromelanin-sensitive MRI and
11
C-PE2I PET, Martín-Bastida
et al.
demonstrate strong linear relationships between these two biomarkers that exist only within the clinically-defined most affected hemisphere.
Parkinson’s disease is characterized by the progressive loss of pigmented dopaminergic neurons in the substantia nigra and associated striatal deafferentation. Neuromelanin content is thought to reflect the loss of pigmented neurons, but available data characterizing its relationship with striatal dopaminergic integrity are not comprehensive or consistent, and predominantly involve heterogeneous samples. In this cross-sectional study, we used neuromelanin-sensitive MRI and the highly specific dopamine transporter PET radioligand,
11
C-PE2I, to assess the association between neuromelanin-containing cell levels in the substantia nigra pars compacta and nigrostriatal terminal density
in vivo
, in 30 patients with bilateral Parkinson’s disease. Fifteen healthy control subjects also underwent neuromelanin-sensitive imaging. We used a novel approach taking into account the anatomical and functional subdivision of substantia nigra into dorsal and ventral tiers and striatal nuclei into pre- and post-commissural subregions, in accordance with previous animal and post-mortem studies, and consider the clinically asymmetric disease presentation.
In vivo
, Parkinson’s disease subjects displayed reduced neuromelanin levels in the ventral (−30 ± 28%) and dorsal tiers (−21 ± 24%) as compared to the control group [
F
(1,43) = 11.95,
P
= 0.001]. Within the Parkinson’s disease group, nigral pigmentation was lower in the ventral tier as compared to the dorsal tier [
F
(1,29) = 36.19,
P
< 0.001] and lower in the clinically-defined most affected side [
F
(1,29) = 4.85,
P
= 0.036]. Similarly, lower dopamine transporter density was observed in the ventral tier [
F
(1,29) = 76.39,
P
< 0.001] and clinically-defined most affected side [
F
(1,29) = 4.21,
P
= 0.049]. Despite similar patterns, regression analysis showed no significant association between nigral pigmentation and nigral dopamine transporter density. However, for the clinically-defined most affected side, significant relationships were observed between pigmentation of the ventral nigral tier with striatal dopamine transporter binding in pre-commissural and post-commissural striatal subregions known to receive nigrostriatal projections from this tier, while the dorsal tier correlated with striatal projection sites in the pre-commissural striatum (
P
< 0.05, Benjamini-Hochberg corrected). In contrast, there were no statistically significant relationships between these two measures in the clinically-defined least affected side. These findings provide important insights into the topography of nigrostriatal neurodegeneration in Parkinson’s disease, indicating that the characteristics of disease progression may fundamentally differ across hemispheres and support post-mortem data showing asynchrony in the loss of neuromelanin-containing versus tyrosine hydroxylase positive nigral cells. Parkinson’s disease is characterized by the progressive loss of pigmented dopaminergic neurons in the substantia nigra and associated striatal deafferentation. Neuromelanin content is thought to reflect the loss of pigmented neurons, but available data characterizing its relationship with striatal dopaminergic integrity are not comprehensive or consistent, and predominantly involve heterogeneous samples. In this cross-sectional study, we used neuromelanin-sensitive MRI and the highly specific dopamine transporter PET radioligand, 11C-PE2I, to assess the association between neuromelanin-containing cell levels in the substantia nigra pars compacta and nigrostriatal terminal density in vivo, in 30 patients with bilateral Parkinson’s disease. Fifteen healthy control subjects also underwent neuromelanin-sensitive imaging. We used a novel approach taking into account the anatomical and functional subdivision of substantia nigra into dorsal and ventral tiers and striatal nuclei into pre- and post-commissural subregions, in accordance with previous animal and post-mortem studies, and consider the clinically asymmetric disease presentation. In vivo, Parkinson’s disease subjects displayed reduced neuromelanin levels in the ventral (−30 ± 28%) and dorsal tiers (−21 ± 24%) as compared to the control group [F(1,43) = 11.95, P = 0.001]. Within the Parkinson’s disease group, nigral pigmentation was lower in the ventral tier as compared to the dorsal tier [F(1,29) = 36.19, P < 0.001] and lower in the clinically-defined most affected side [F(1,29) = 4.85, P = 0.036]. Similarly, lower dopamine transporter density was observed in the ventral tier [F(1,29) = 76.39, P < 0.001] and clinically-defined most affected side [F(1,29) = 4.21, P = 0.049]. Despite similar patterns, regression analysis showed no significant association between nigral pigmentation and nigral dopamine transporter density. However, for the clinically-defined most affected side, significant relationships were observed between pigmentation of the ventral nigral tier with striatal dopamine transporter binding in pre-commissural and post-commissural striatal subregions known to receive nigrostriatal projections from this tier, while the dorsal tier correlated with striatal projection sites in the pre-commissural striatum (P < 0.05, Benjamini-Hochberg corrected). In contrast, there were no statistically significant relationships between these two measures in the clinically-defined least affected side. These findings provide important insights into the topography of nigrostriatal neurodegeneration in Parkinson’s disease, indicating that the characteristics of disease progression may fundamentally differ across hemispheres and support post-mortem data showing asynchrony in the loss of neuromelanin-containing versus tyrosine hydroxylase positive nigral cells. Parkinson's disease is characterized by the progressive loss of pigmented dopaminergic neurons in the substantia nigra and associated striatal deafferentation. Neuromelanin content is thought to reflect the loss of pigmented neurons, but available data characterizing its relationship with striatal dopaminergic integrity are not comprehensive or consistent, and predominantly involve heterogeneous samples. In this cross-sectional study, we used neuromelanin-sensitive MRI and the highly specific dopamine transporter PET radioligand, 11C-PE2I, to assess the association between neuromelanin-containing cell levels in the substantia nigra pars compacta and nigrostriatal terminal density in vivo, in 30 patients with bilateral Parkinson's disease. Fifteen healthy control subjects also underwent neuromelanin-sensitive imaging. We used a novel approach taking into account the anatomical and functional subdivision of substantia nigra into dorsal and ventral tiers and striatal nuclei into pre- and post-commissural subregions, in accordance with previous animal and post-mortem studies, and consider the clinically asymmetric disease presentation. In vivo, Parkinson's disease subjects displayed reduced neuromelanin levels in the ventral (-30 ± 28%) and dorsal tiers (-21 ± 24%) as compared to the control group [F(1,43) = 11.95, P = 0.001]. Within the Parkinson's disease group, nigral pigmentation was lower in the ventral tier as compared to the dorsal tier [F(1,29) = 36.19, P < 0.001] and lower in the clinically-defined most affected side [F(1,29) = 4.85, P = 0.036]. Similarly, lower dopamine transporter density was observed in the ventral tier [F(1,29) = 76.39, P < 0.001] and clinically-defined most affected side [F(1,29) = 4.21, P = 0.049]. Despite similar patterns, regression analysis showed no significant association between nigral pigmentation and nigral dopamine transporter density. However, for the clinically-defined most affected side, significant relationships were observed between pigmentation of the ventral nigral tier with striatal dopamine transporter binding in pre-commissural and post-commissural striatal subregions known to receive nigrostriatal projections from this tier, while the dorsal tier correlated with striatal projection sites in the pre-commissural striatum (P < 0.05, Benjamini-Hochberg corrected). In contrast, there were no statistically significant relationships between these two measures in the clinically-defined least affected side. These findings provide important insights into the topography of nigrostriatal neurodegeneration in Parkinson's disease, indicating that the characteristics of disease progression may fundamentally differ across hemispheres and support post-mortem data showing asynchrony in the loss of neuromelanin-containing versus tyrosine hydroxylase positive nigral cells.Parkinson's disease is characterized by the progressive loss of pigmented dopaminergic neurons in the substantia nigra and associated striatal deafferentation. Neuromelanin content is thought to reflect the loss of pigmented neurons, but available data characterizing its relationship with striatal dopaminergic integrity are not comprehensive or consistent, and predominantly involve heterogeneous samples. In this cross-sectional study, we used neuromelanin-sensitive MRI and the highly specific dopamine transporter PET radioligand, 11C-PE2I, to assess the association between neuromelanin-containing cell levels in the substantia nigra pars compacta and nigrostriatal terminal density in vivo, in 30 patients with bilateral Parkinson's disease. Fifteen healthy control subjects also underwent neuromelanin-sensitive imaging. We used a novel approach taking into account the anatomical and functional subdivision of substantia nigra into dorsal and ventral tiers and striatal nuclei into pre- and post-commissural subregions, in accordance with previous animal and post-mortem studies, and consider the clinically asymmetric disease presentation. In vivo, Parkinson's disease subjects displayed reduced neuromelanin levels in the ventral (-30 ± 28%) and dorsal tiers (-21 ± 24%) as compared to the control group [F(1,43) = 11.95, P = 0.001]. Within the Parkinson's disease group, nigral pigmentation was lower in the ventral tier as compared to the dorsal tier [F(1,29) = 36.19, P < 0.001] and lower in the clinically-defined most affected side [F(1,29) = 4.85, P = 0.036]. Similarly, lower dopamine transporter density was observed in the ventral tier [F(1,29) = 76.39, P < 0.001] and clinically-defined most affected side [F(1,29) = 4.21, P = 0.049]. Despite similar patterns, regression analysis showed no significant association between nigral pigmentation and nigral dopamine transporter density. However, for the clinically-defined most affected side, significant relationships were observed between pigmentation of the ventral nigral tier with striatal dopamine transporter binding in pre-commissural and post-commissural striatal subregions known to receive nigrostriatal projections from this tier, while the dorsal tier correlated with striatal projection sites in the pre-commissural striatum (P < 0.05, Benjamini-Hochberg corrected). In contrast, there were no statistically significant relationships between these two measures in the clinically-defined least affected side. These findings provide important insights into the topography of nigrostriatal neurodegeneration in Parkinson's disease, indicating that the characteristics of disease progression may fundamentally differ across hemispheres and support post-mortem data showing asynchrony in the loss of neuromelanin-containing versus tyrosine hydroxylase positive nigral cells. Parkinson's disease is characterized by the progressive loss of pigmented dopaminergic neurons in the substantia nigra and associated striatal deafferentation. Neuromelanin content is thought to reflect the loss of pigmented neurons, but available data characterizing its relationship with striatal dopaminergic integrity are not comprehensive or consistent, and predominantly involve heterogeneous samples. In this cross-sectional study, we used neuromelanin-sensitive MRI and the highly specific dopamine transporter PET radioligand, 11C-PE2I, to assess the association between neuromelanin-containing cell levels in the substantia nigra pars compacta and nigrostriatal terminal density in vivo, in 30 patients with bilateral Parkinson's disease. Fifteen healthy control subjects also underwent neuromelanin-sensitive imaging. We used a novel approach taking into account the anatomical and functional subdivision of substantia nigra into dorsal and ventral tiers and striatal nuclei into pre- and post-commissural subregions, in accordance with previous animal and post-mortem studies, and consider the clinically asymmetric disease presentation. In vivo, Parkinson's disease subjects displayed reduced neuromelanin levels in the ventral (-30 ± 28%) and dorsal tiers (-21 ± 24%) as compared to the control group [F(1,43) = 11.95, P = 0.001]. Within the Parkinson's disease group, nigral pigmentation was lower in the ventral tier as compared to the dorsal tier [F(1,29) = 36.19, P < 0.001] and lower in the clinically-defined most affected side [F(1,29) = 4.85, P = 0.036]. Similarly, lower dopamine transporter density was observed in the ventral tier [F(1,29) = 76.39, P < 0.001] and clinically-defined most affected side [F(1,29) = 4.21, P = 0.049]. Despite similar patterns, regression analysis showed no significant association between nigral pigmentation and nigral dopamine transporter density. However, for the clinically-defined most affected side, significant relationships were observed between pigmentation of the ventral nigral tier with striatal dopamine transporter binding in pre-commissural and post-commissural striatal subregions known to receive nigrostriatal projections from this tier, while the dorsal tier correlated with striatal projection sites in the pre-commissural striatum (P < 0.05, Benjamini-Hochberg corrected). In contrast, there were no statistically significant relationships between these two measures in the clinically-defined least affected side. These findings provide important insights into the topography of nigrostriatal neurodegeneration in Parkinson's disease, indicating that the characteristics of disease progression may fundamentally differ across hemispheres and support post-mortem data showing asynchrony in the loss of neuromelanin-containing versus tyrosine hydroxylase positive nigral cells. |
| Author | Barker, Roger A Piccini, Paola Gunn, Roger N Xing, Yue Martín-Bastida, Antonio Roussakis, Andreas Antonios Searle, Graham E Schwarz, Stefan T Auer, Dorothee P Lao-Kaim, Nicholas P |
| AuthorAffiliation | 2 Neurology Department, Clinica Universidad de Navarra, Pamplona, Navarra, Spain 5 Centre for Restorative Neuroscience, Centre for Neuroinflammation and Neurodegeneration, Division of Brain Sciences, Imperial College London, London, UK 4 Radiological Sciences, Division of Clinical Neuroscience, University of Nottingham, Queen’s Medical Centre, Nottingham, UK 6 John Van Geest Centre for Brain Repair, University of Cambridge, Cambridge, UK 3 Invicro LLC, London, UK 1 Centre for Neuroinflammation and Neurodegeneration, Division of Brain Sciences, Imperial College London, London, UK |
| AuthorAffiliation_xml | – name: 1 Centre for Neuroinflammation and Neurodegeneration, Division of Brain Sciences, Imperial College London, London, UK – name: 6 John Van Geest Centre for Brain Repair, University of Cambridge, Cambridge, UK – name: 2 Neurology Department, Clinica Universidad de Navarra, Pamplona, Navarra, Spain – name: 4 Radiological Sciences, Division of Clinical Neuroscience, University of Nottingham, Queen’s Medical Centre, Nottingham, UK – name: 3 Invicro LLC, London, UK – name: 5 Centre for Restorative Neuroscience, Centre for Neuroinflammation and Neurodegeneration, Division of Brain Sciences, Imperial College London, London, UK |
| Author_xml | – sequence: 1 givenname: Antonio surname: Martín-Bastida fullname: Martín-Bastida, Antonio organization: Centre for Neuroinflammation and Neurodegeneration, Division of Brain Sciences, Imperial College London, London, UK, Neurology Department, Clinica Universidad de Navarra, Pamplona, Navarra, Spain – sequence: 2 givenname: Nicholas P orcidid: 0000-0002-0241-7630 surname: Lao-Kaim fullname: Lao-Kaim, Nicholas P organization: Centre for Neuroinflammation and Neurodegeneration, Division of Brain Sciences, Imperial College London, London, UK – sequence: 3 givenname: Andreas Antonios surname: Roussakis fullname: Roussakis, Andreas Antonios organization: Centre for Neuroinflammation and Neurodegeneration, Division of Brain Sciences, Imperial College London, London, UK – sequence: 4 givenname: Graham E surname: Searle fullname: Searle, Graham E organization: Invicro LLC, London, UK – sequence: 5 givenname: Yue surname: Xing fullname: Xing, Yue organization: Radiological Sciences, Division of Clinical Neuroscience, University of Nottingham, Queen’s Medical Centre, Nottingham, UK – sequence: 6 givenname: Roger N surname: Gunn fullname: Gunn, Roger N organization: Invicro LLC, London, UK, Centre for Restorative Neuroscience, Centre for Neuroinflammation and Neurodegeneration, Division of Brain Sciences, Imperial College London, London, UK – sequence: 7 givenname: Stefan T surname: Schwarz fullname: Schwarz, Stefan T organization: Radiological Sciences, Division of Clinical Neuroscience, University of Nottingham, Queen’s Medical Centre, Nottingham, UK – sequence: 8 givenname: Roger A surname: Barker fullname: Barker, Roger A organization: John Van Geest Centre for Brain Repair, University of Cambridge, Cambridge, UK – sequence: 9 givenname: Dorothee P surname: Auer fullname: Auer, Dorothee P organization: Radiological Sciences, Division of Clinical Neuroscience, University of Nottingham, Queen’s Medical Centre, Nottingham, UK – sequence: 10 givenname: Paola orcidid: 0000-0003-4162-6141 surname: Piccini fullname: Piccini, Paola organization: Centre for Neuroinflammation and Neurodegeneration, Division of Brain Sciences, Imperial College London, London, UK |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/31056699$$D View this record in MEDLINE/PubMed |
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| DOI | 10.1093/brain/awz120 |
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| ISSN | 0006-8950 1460-2156 |
| IngestDate | Thu Aug 21 14:00:59 EDT 2025 Fri Jul 11 11:11:35 EDT 2025 Sat May 31 02:12:26 EDT 2025 Thu Apr 24 22:53:27 EDT 2025 Tue Jul 01 00:46:10 EDT 2025 |
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| Issue | 7 |
| Keywords | magnetic resonance imaging dopamine transporter positron emission tomography Parkinson’s disease neuromelanin |
| Language | English |
| License | https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model The Author(s) (2019). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oup.com. This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model) |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Antonio Martín-Bastida and Nicholas P. Lao-Kaim authors contributed equally to this work. |
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| Snippet | Parkinson’s disease is characterized by the progressive loss of pigmented dopaminergic neurons in the substantia nigra and associated striatal deafferentation.... Parkinson's disease is characterized by the progressive loss of pigmented dopaminergic neurons in the substantia nigra and associated striatal deafferentation.... Striatal dopamine transporter density and nigral neuromelanin content are imaging biomarkers of nigrostriatal denervation and disease progression in... |
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| SubjectTerms | Case-Control Studies Corpus Striatum - anatomy & histology Corpus Striatum - metabolism Cross-Sectional Studies Dopamine - metabolism Female Humans Magnetic Resonance Imaging Male Melanins - metabolism Middle Aged Nerve Endings - metabolism Neuroimaging Nortropanes - metabolism Original Positron-Emission Tomography Substantia Nigra - anatomy & histology Substantia Nigra - metabolism |
| Title | Relationship between neuromelanin and dopamine terminals within the Parkinson’s nigrostriatal system |
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