Evidence from spatial pattern analysis for the anatomical spread of α-synuclein pathology in Parkinson's disease dementia

Richard A. Armstrong

doi:10.5114/fn.2017.66710

Evidence from spatial pattern analysis for the anatomical spread of α-synuclein pathology in Parkinson's disease dementia

Richard A. Armstrong^*

^*Corresponding author for this work

Research output: Contribution to journal › Article › peer-review

Abstract

The objective of this study was to determine whether there is evidence from quantitative morphometry and spatial pattern analysis to support the hypothesis of anatomical spread of α-synuclein in Parkinson's disease dementia (PDD). Hence, clustering of α-synuclein-immunoreactive Lewy bodies (LB), Lewy neurites (LN), and Lewy grains (LG) was studied in α-synuclein-immunolabeled sections of cortical and limbic regions in 12 cases of PDD. The data suggested that: (1) LB, LN, and LG occurred in clusters which in 63% of regions were regularly distributed parallel to the tissue boundary, (2) in approximately 30% of cortical regions, the estimated cluster size of LB, LN, and LG was within the size range of cellular columns associated with the cortico-cortical pathways, (3) regularly distributed clusters were present in anatomically connected regions, and (4) the clustering pattern was similar to that of prion protein (PrPsc) deposits in Creutzfeldt-Jacob disease (CJD). The clustering patterns of LB, LN, and LG were similar to those exhibited by cellular inclusions in other synucleinopathies and by PrPsc deposits in prion disease and therefore, anatomical spread of pathogenic α-synuclein could be involved in the pathogenesis of PDD.

Original language	English
Pages (from-to)	23-30
Number of pages	8
Journal	Folia Neuropathologica
Volume	55
Issue number	1
DOIs	https://doi.org/10.5114/fn.2017.66710
Publication status	Published - 27 Mar 2017

Bibliographical note

© 2017 Mossakowski Medical Research Centre Polish Academy of Sciences and the Polish Association of Neuropathologists. This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) License (http://creativecommons.org/licenses/by-nc-sa/4.0/), allowing third parties to copy and redistribute the material in any medium or format and to remix, transform, and build upon the material, provided the original work is properly cited and states its license.

Keywords

anatomical spread
Lewy body (LB)
Lewy grain (lg)
Lewy neurite (LN)
Parkinson disease dementia (PDD)
spatial pattern
synucleinopathy

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10.5114/fn.2017.66710Licence: CC BY-NC-SA 3.0

Anatomical spread of alpha-synuclein pathology in Parkinson's disease dementia
© 2017 Mossakowski Medical Research Centre Polish Academy of Sciences and the Polish Association of Neuropathologists. This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) License (http://creativecommons.org/licenses/by-nc-sa/4.0/), allowing third parties to copy and redistribute the material in any medium or format and to remix, transform, and build upon the material, provided the original work is properly cited and states its license.
Final published version, 129 KBLicence: CC BY-NC-SA 3.0

Cite this

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title = "Evidence from spatial pattern analysis for the anatomical spread of α-synuclein pathology in Parkinson's disease dementia",

abstract = "The objective of this study was to determine whether there is evidence from quantitative morphometry and spatial pattern analysis to support the hypothesis of anatomical spread of α-synuclein in Parkinson's disease dementia (PDD). Hence, clustering of α-synuclein-immunoreactive Lewy bodies (LB), Lewy neurites (LN), and Lewy grains (LG) was studied in α-synuclein-immunolabeled sections of cortical and limbic regions in 12 cases of PDD. The data suggested that: (1) LB, LN, and LG occurred in clusters which in 63% of regions were regularly distributed parallel to the tissue boundary, (2) in approximately 30% of cortical regions, the estimated cluster size of LB, LN, and LG was within the size range of cellular columns associated with the cortico-cortical pathways, (3) regularly distributed clusters were present in anatomically connected regions, and (4) the clustering pattern was similar to that of prion protein (PrPsc) deposits in Creutzfeldt-Jacob disease (CJD). The clustering patterns of LB, LN, and LG were similar to those exhibited by cellular inclusions in other synucleinopathies and by PrPsc deposits in prion disease and therefore, anatomical spread of pathogenic α-synuclein could be involved in the pathogenesis of PDD.",

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AB - The objective of this study was to determine whether there is evidence from quantitative morphometry and spatial pattern analysis to support the hypothesis of anatomical spread of α-synuclein in Parkinson's disease dementia (PDD). Hence, clustering of α-synuclein-immunoreactive Lewy bodies (LB), Lewy neurites (LN), and Lewy grains (LG) was studied in α-synuclein-immunolabeled sections of cortical and limbic regions in 12 cases of PDD. The data suggested that: (1) LB, LN, and LG occurred in clusters which in 63% of regions were regularly distributed parallel to the tissue boundary, (2) in approximately 30% of cortical regions, the estimated cluster size of LB, LN, and LG was within the size range of cellular columns associated with the cortico-cortical pathways, (3) regularly distributed clusters were present in anatomically connected regions, and (4) the clustering pattern was similar to that of prion protein (PrPsc) deposits in Creutzfeldt-Jacob disease (CJD). The clustering patterns of LB, LN, and LG were similar to those exhibited by cellular inclusions in other synucleinopathies and by PrPsc deposits in prion disease and therefore, anatomical spread of pathogenic α-synuclein could be involved in the pathogenesis of PDD.

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IS - 1

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Evidence from spatial pattern analysis for the anatomical spread of α-synuclein pathology in Parkinson's disease dementia

Abstract

Bibliographical note

Keywords

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