Disease progression modelling reveals heterogeneity in trajectories of Lewy-type α-synuclein pathology

Lewy body (LB) diseases, characterized by the aggregation of misfolded α-synuclein proteins, exhibit notable clinical heterogeneity. This may be due to variations in accumulation patterns of LB neuropathology. Here we apply a data-driven disease progression model to regional neuropathological LB den...

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Published inNature communications Vol. 15; no. 1; pp. 5133 - 15
Main Authors Mastenbroek, Sophie E., Vogel, Jacob W., Collij, Lyduine E., Serrano, Geidy E., Tremblay, Cécilia, Young, Alexandra L., Arce, Richard A., Shill, Holly A., Driver-Dunckley, Erika D., Mehta, Shyamal H., Belden, Christine M., Atri, Alireza, Choudhury, Parichita, Barkhof, Frederik, Adler, Charles H., Ossenkoppele, Rik, Beach, Thomas G., Hansson, Oskar
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 15.06.2024
Nature Publishing Group
Nature Portfolio
Subjects
631/378/116/2396
631/378/1689
692/699/375/365/1283
692/699/375/365/1718
Abnormalities
Accumulation
Aged
Aged, 80 and over
alpha-Synuclein - metabolism
Alzheimer Disease - metabolism
Alzheimer Disease - pathology
Alzheimer's disease
Brain
Brain - metabolism
Brain - pathology
Brain stem
Brain Stem - metabolism
Brain Stem - pathology
Clinical Laboratory Medicine
Clinical Medicine
Disease
Disease Progression
Female
Heterogeneity
Humanities and Social Sciences
Humans
Klinisk laboratoriemedicin
Klinisk medicin
Lewy bodies
Lewy Bodies - metabolism
Lewy Bodies - pathology
Lewy body disease
Lewy Body Disease - metabolism
Lewy Body Disease - pathology
Male
Medical and Health Sciences
Medicin och hälsovetenskap
Middle Aged
multidisciplinary
Neurodegenerative diseases
Olfactory bulb
Olfactory Bulb - metabolism
Olfactory Bulb - pathology
Pathology
Science
Science (multidisciplinary)
Synuclein
Online AccessGet full text
ISSN2041-1723
2041-1723
DOI10.1038/s41467-024-49402-x

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Abstract Lewy body (LB) diseases, characterized by the aggregation of misfolded α-synuclein proteins, exhibit notable clinical heterogeneity. This may be due to variations in accumulation patterns of LB neuropathology. Here we apply a data-driven disease progression model to regional neuropathological LB density scores from 814 brain donors with Lewy pathology. We describe three inferred trajectories of LB pathology that are characterized by differing clinicopathological presentation and longitudinal antemortem clinical progression. Most donors (81.9%) show earliest pathology in the olfactory bulb, followed by accumulation in either limbic (60.8%) or brainstem (21.1%) regions. The remaining donors (18.1%) initially exhibit abnormalities in brainstem regions. Early limbic pathology is associated with Alzheimer’s disease-associated characteristics while early brainstem pathology is associated with progressive motor impairment and substantial LB pathology outside of the brain. Our data provides evidence for heterogeneity in the temporal spread of LB pathology, possibly explaining some of the clinical disparities observed in Lewy body disease. Lewy body diseases exhibit notable clinical and pathological heterogeneity. Here, the authors found three distinct trajectories of Lewy body pathology that are associated with different clinicopathological characteristics.
AbstractList Lewy body (LB) diseases, characterized by the aggregation of misfolded α-synuclein proteins, exhibit notable clinical heterogeneity. This may be due to variations in accumulation patterns of LB neuropathology. Here we apply a data-driven disease progression model to regional neuropathological LB density scores from 814 brain donors with Lewy pathology. We describe three inferred trajectories of LB pathology that are characterized by differing clinicopathological presentation and longitudinal antemortem clinical progression. Most donors (81.9%) show earliest pathology in the olfactory bulb, followed by accumulation in either limbic (60.8%) or brainstem (21.1%) regions. The remaining donors (18.1%) initially exhibit abnormalities in brainstem regions. Early limbic pathology is associated with Alzheimer’s disease-associated characteristics while early brainstem pathology is associated with progressive motor impairment and substantial LB pathology outside of the brain. Our data provides evidence for heterogeneityin the temporal spread of LB pathology, possibly explaining some of the clinical disparities observed in Lewy body disease.
Lewy body (LB) diseases, characterized by the aggregation of misfolded α-synuclein proteins, exhibit notable clinical heterogeneity. This may be due to variations in accumulation patterns of LB neuropathology. Here we apply a data-driven disease progression model to regional neuropathological LB density scores from 814 brain donors with Lewy pathology. We describe three inferred trajectories of LB pathology that are characterized by differing clinicopathological presentation and longitudinal antemortem clinical progression. Most donors (81.9%) show earliest pathology in the olfactory bulb, followed by accumulation in either limbic (60.8%) or brainstem (21.1%) regions. The remaining donors (18.1%) initially exhibit abnormalities in brainstem regions. Early limbic pathology is associated with Alzheimer’s disease-associated characteristics while early brainstem pathology is associated with progressive motor impairment and substantial LB pathology outside of the brain. Our data provides evidence for heterogeneity in the temporal spread of LB pathology, possibly explaining some of the clinical disparities observed in Lewy body disease. Lewy body diseases exhibit notable clinical and pathological heterogeneity. Here, the authors found three distinct trajectories of Lewy body pathology that are associated with different clinicopathological characteristics.
Lewy body (LB) diseases, characterized by the aggregation of misfolded α-synuclein proteins, exhibit notable clinical heterogeneity. This may be due to variations in accumulation patterns of LB neuropathology. Here we apply a data-driven disease progression model to regional neuropathological LB density scores from 814 brain donors with Lewy pathology. We describe three inferred trajectories of LB pathology that are characterized by differing clinicopathological presentation and longitudinal antemortem clinical progression. Most donors (81.9%) show earliest pathology in the olfactory bulb, followed by accumulation in either limbic (60.8%) or brainstem (21.1%) regions. The remaining donors (18.1%) initially exhibit abnormalities in brainstem regions. Early limbic pathology is associated with Alzheimer's disease-associated characteristics while early brainstem pathology is associated with progressive motor impairment and substantial LB pathology outside of the brain. Our data provides evidence for heterogeneity in the temporal spread of LB pathology, possibly explaining some of the clinical disparities observed in Lewy body disease.
Lewy body (LB) diseases, characterized by the aggregation of misfolded α-synuclein proteins, exhibit notable clinical heterogeneity. This may be due to variations in accumulation patterns of LB neuropathology. Here we apply a data-driven disease progression model to regional neuropathological LB density scores from 814 brain donors with Lewy pathology. We describe three inferred trajectories of LB pathology that are characterized by differing clinicopathological presentation and longitudinal antemortem clinical progression. Most donors (81.9%) show earliest pathology in the olfactory bulb, followed by accumulation in either limbic (60.8%) or brainstem (21.1%) regions. The remaining donors (18.1%) initially exhibit abnormalities in brainstem regions. Early limbic pathology is associated with Alzheimer's disease-associated characteristics while early brainstem pathology is associated with progressive motor impairment and substantial LB pathology outside of the brain. Our data provides evidence for heterogeneity in the temporal spread of LB pathology, possibly explaining some of the clinical disparities observed in Lewy body disease.Lewy body (LB) diseases, characterized by the aggregation of misfolded α-synuclein proteins, exhibit notable clinical heterogeneity. This may be due to variations in accumulation patterns of LB neuropathology. Here we apply a data-driven disease progression model to regional neuropathological LB density scores from 814 brain donors with Lewy pathology. We describe three inferred trajectories of LB pathology that are characterized by differing clinicopathological presentation and longitudinal antemortem clinical progression. Most donors (81.9%) show earliest pathology in the olfactory bulb, followed by accumulation in either limbic (60.8%) or brainstem (21.1%) regions. The remaining donors (18.1%) initially exhibit abnormalities in brainstem regions. Early limbic pathology is associated with Alzheimer's disease-associated characteristics while early brainstem pathology is associated with progressive motor impairment and substantial LB pathology outside of the brain. Our data provides evidence for heterogeneity in the temporal spread of LB pathology, possibly explaining some of the clinical disparities observed in Lewy body disease.
Abstract Lewy body (LB) diseases, characterized by the aggregation of misfolded α-synuclein proteins, exhibit notable clinical heterogeneity. This may be due to variations in accumulation patterns of LB neuropathology. Here we apply a data-driven disease progression model to regional neuropathological LB density scores from 814 brain donors with Lewy pathology. We describe three inferred trajectories of LB pathology that are characterized by differing clinicopathological presentation and longitudinal antemortem clinical progression. Most donors (81.9%) show earliest pathology in the olfactory bulb, followed by accumulation in either limbic (60.8%) or brainstem (21.1%) regions. The remaining donors (18.1%) initially exhibit abnormalities in brainstem regions. Early limbic pathology is associated with Alzheimer’s disease-associated characteristics while early brainstem pathology is associated with progressive motor impairment and substantial LB pathology outside of the brain. Our data provides evidence for heterogeneity in the temporal spread of LB pathology, possibly explaining some of the clinical disparities observed in Lewy body disease.
Lewy body (LB) diseases, characterized by the aggregation of misfolded α-synuclein proteins, exhibit notable clinical heterogeneity. This may be due to variations in accumulation patterns of LB neuropathology. Here we apply a data-driven disease progression model to regional neuropathological LB density scores from 814 brain donors with Lewy pathology. We describe three inferred trajectories of LB pathology that are characterized by differing clinicopathological presentation and longitudinal antemortem clinical progression. Most donors (81.9%) show earliest pathology in the olfactory bulb, followed by accumulation in either limbic (60.8%) or brainstem (21.1%) regions. The remaining donors (18.1%) initially exhibit abnormalities in brainstem regions. Early limbic pathology is associated with Alzheimer’s disease-associated characteristics while early brainstem pathology is associated with progressive motor impairment and substantial LB pathology outside of the brain. Our data provides evidence for heterogeneity in the temporal spread of LB pathology, possibly explaining some of the clinical disparities observed in Lewy body disease.Lewy body diseases exhibit notable clinical and pathological heterogeneity. Here, the authors found three distinct trajectories of Lewy body pathology that are associated with different clinicopathological characteristics.
ArticleNumber 5133
Author Vogel, Jacob W.
Choudhury, Parichita
Ossenkoppele, Rik
Mehta, Shyamal H.
Young, Alexandra L.
Collij, Lyduine E.
Tremblay, Cécilia
Belden, Christine M.
Hansson, Oskar
Shill, Holly A.
Serrano, Geidy E.
Driver-Dunckley, Erika D.
Atri, Alireza
Beach, Thomas G.
Barkhof, Frederik
Adler, Charles H.
Mastenbroek, Sophie E.
Arce, Richard A.
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/38879548$$D View this record in MEDLINE/PubMed
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The Author(s) 2024. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.
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Snippet Lewy body (LB) diseases, characterized by the aggregation of misfolded α-synuclein proteins, exhibit notable clinical heterogeneity. This may be due to...
Abstract Lewy body (LB) diseases, characterized by the aggregation of misfolded α-synuclein proteins, exhibit notable clinical heterogeneity. This may be due...
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631/378/1689
692/699/375/365/1283
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Abnormalities
Accumulation
Aged
Aged, 80 and over
alpha-Synuclein - metabolism
Alzheimer Disease - metabolism
Alzheimer Disease - pathology
Alzheimer's disease
Brain
Brain - metabolism
Brain - pathology
Brain stem
Brain Stem - metabolism
Brain Stem - pathology
Clinical Laboratory Medicine
Clinical Medicine
Disease
Disease Progression
Female
Heterogeneity
Humanities and Social Sciences
Humans
Klinisk laboratoriemedicin
Klinisk medicin
Lewy bodies
Lewy Bodies - metabolism
Lewy Bodies - pathology
Lewy body disease
Lewy Body Disease - metabolism
Lewy Body Disease - pathology
Male
Medical and Health Sciences
Medicin och hälsovetenskap
Middle Aged
multidisciplinary
Neurodegenerative diseases
Olfactory bulb
Olfactory Bulb - metabolism
Olfactory Bulb - pathology
Pathology
Science
Science (multidisciplinary)
Synuclein
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Title Disease progression modelling reveals heterogeneity in trajectories of Lewy-type α-synuclein pathology
URI https://link.springer.com/article/10.1038/s41467-024-49402-x
https://www.ncbi.nlm.nih.gov/pubmed/38879548
https://www.proquest.com/docview/3068493888
https://www.proquest.com/docview/3068757977
https://pubmed.ncbi.nlm.nih.gov/PMC11180185
https://doaj.org/article/8ead8da20952462faeaafda287e2a07f
Volume 15
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