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Lateralized ante mortem and post mortem pathology in a case of Lewy body disease with corticobasal syndrome

INTRODUCTION: Lewy body diseases are pathologically characterized by α‐synuclein pathology. Alzheimer's disease (AD) co‐pathology can influence phenotypes. In vivo AD biomarkers can suggest the presence of this co‐pathology in unusual cases, but pathological validation remains essential. METHOD...

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Autores principales: Coughlin, David G., Coslett, H. Branch, Peterson, Claire, Phillips, Jeffrey S., McMillan, Corey, Lee, Edward B., Trojanowski, John Q., Grossman, Murray, Irwin, David J.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9092750/
https://www.ncbi.nlm.nih.gov/pubmed/35592691
http://dx.doi.org/10.1002/trc2.12294
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author Coughlin, David G.
Coslett, H. Branch
Peterson, Claire
Phillips, Jeffrey S.
McMillan, Corey
Lee, Edward B.
Trojanowski, John Q.
Grossman, Murray
Irwin, David J.
author_facet Coughlin, David G.
Coslett, H. Branch
Peterson, Claire
Phillips, Jeffrey S.
McMillan, Corey
Lee, Edward B.
Trojanowski, John Q.
Grossman, Murray
Irwin, David J.
author_sort Coughlin, David G.
collection PubMed
description INTRODUCTION: Lewy body diseases are pathologically characterized by α‐synuclein pathology. Alzheimer's disease (AD) co‐pathology can influence phenotypes. In vivo AD biomarkers can suggest the presence of this co‐pathology in unusual cases, but pathological validation remains essential. METHODS: This patient originally presented with corticobasal syndrome and later developed visual hallucinations and parkinsonism consistent with a synucleinopathy. The patient underwent CSF sampling, 18F‐flortaucipir PET scanning, and brain donation with bilateral regions available for digital histological analysis. RESULTS: CSF Aβ42 and t‐tau were in the AD range. 18F‐flortaucipir scanning showed right‐lateralized retention in all lobes (t = 4.3‐10.0, P < .006). Neocortical stage Lewy body pathology and high levels of AD neuropathological changes were present at autopsy. There was right lateralization of α‐synuclein and tau pathology (T value = 3.1, P value = .007 and T value = 3.3, P value = .004 respectively). DISCUSSION: This case with overlapping tauopathy and synucleinopathy clinical features had in‐depth biomarker characterization and rare bilateral post‐mortem sampling showing lateralized tau and α‐synuclein pathology suggesting possible synergistic relationships.
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spelling pubmed-90927502022-05-18 Lateralized ante mortem and post mortem pathology in a case of Lewy body disease with corticobasal syndrome Coughlin, David G. Coslett, H. Branch Peterson, Claire Phillips, Jeffrey S. McMillan, Corey Lee, Edward B. Trojanowski, John Q. Grossman, Murray Irwin, David J. Alzheimers Dement (N Y) Short Report INTRODUCTION: Lewy body diseases are pathologically characterized by α‐synuclein pathology. Alzheimer's disease (AD) co‐pathology can influence phenotypes. In vivo AD biomarkers can suggest the presence of this co‐pathology in unusual cases, but pathological validation remains essential. METHODS: This patient originally presented with corticobasal syndrome and later developed visual hallucinations and parkinsonism consistent with a synucleinopathy. The patient underwent CSF sampling, 18F‐flortaucipir PET scanning, and brain donation with bilateral regions available for digital histological analysis. RESULTS: CSF Aβ42 and t‐tau were in the AD range. 18F‐flortaucipir scanning showed right‐lateralized retention in all lobes (t = 4.3‐10.0, P < .006). Neocortical stage Lewy body pathology and high levels of AD neuropathological changes were present at autopsy. There was right lateralization of α‐synuclein and tau pathology (T value = 3.1, P value = .007 and T value = 3.3, P value = .004 respectively). DISCUSSION: This case with overlapping tauopathy and synucleinopathy clinical features had in‐depth biomarker characterization and rare bilateral post‐mortem sampling showing lateralized tau and α‐synuclein pathology suggesting possible synergistic relationships. John Wiley and Sons Inc. 2022-05-11 /pmc/articles/PMC9092750/ /pubmed/35592691 http://dx.doi.org/10.1002/trc2.12294 Text en © 2022 The Authors. Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring published by Wiley Periodicals, LLC on behalf of Alzheimer's Association https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.
spellingShingle Short Report
Coughlin, David G.
Coslett, H. Branch
Peterson, Claire
Phillips, Jeffrey S.
McMillan, Corey
Lee, Edward B.
Trojanowski, John Q.
Grossman, Murray
Irwin, David J.
Lateralized ante mortem and post mortem pathology in a case of Lewy body disease with corticobasal syndrome
title Lateralized ante mortem and post mortem pathology in a case of Lewy body disease with corticobasal syndrome
title_full Lateralized ante mortem and post mortem pathology in a case of Lewy body disease with corticobasal syndrome
title_fullStr Lateralized ante mortem and post mortem pathology in a case of Lewy body disease with corticobasal syndrome
title_full_unstemmed Lateralized ante mortem and post mortem pathology in a case of Lewy body disease with corticobasal syndrome
title_short Lateralized ante mortem and post mortem pathology in a case of Lewy body disease with corticobasal syndrome
title_sort lateralized ante mortem and post mortem pathology in a case of lewy body disease with corticobasal syndrome
topic Short Report
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9092750/
https://www.ncbi.nlm.nih.gov/pubmed/35592691
http://dx.doi.org/10.1002/trc2.12294
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