Aquaporin-4 mis-localization slows glymphatic clearance of α-synuclein and promotes α-synuclein pathology and aggregate propagation Article Swipe
Molly Braun
,
Matthew Simon
,
Jay Jang
,
Keith Sanderson
,
J Swierz
,
Mathew Sevao
,
Alexandra Pincus
,
Allison J. Schaser
,
Jonathan E. Elliott
,
Miranda M. Lim
,
Vivek K. Unni
,
Abigail G. Schindler
,
C. Dirk Keene
,
Caitlin S. Latimer
,
Jeffrey J. Iliff
·
YOU?
·
· 2024
· Open Access
·
· DOI: https://doi.org/10.1101/2024.08.14.607971
YOU?
·
· 2024
· Open Access
·
· DOI: https://doi.org/10.1101/2024.08.14.607971
The appearance of misfolded and aggregated proteins is a pathological hallmark of numerous neurodegenerative diseases including Alzheimer's disease and Parkinson's disease. Sleep disruption is proposed to contribute to these pathological processes and is a common early feature among neurodegenerative disorders. Synucleinopathies are a subclass of neurodegenerative conditions defined by the presence of α-synuclein aggregates, which may not only enhance cell death, but also contribute to disease progression by seeding the formation of additional aggregates in neighboring cells. The mechanisms driving intercellular transmission of aggregates remains unclear. We propose that disruption of sleep-active glymphatic function, caused by loss of precise perivascular AQP4 localization, inhibits α-synuclein clearance and facilitates α-synuclein propagation and seeding. We examined human post-mortem frontal cortex and found that neocortical α-synuclein pathology was associated with AQP4 mis-localization throughout the gray matter. Using a transgenic mouse model lacking the adapter protein α-syntrophin, we observed that loss of perivascular AQP4 localization impairs the glymphatic clearance of α-synuclein from intersititial to cerebrospinal fluid. Using a mouse model of α-synuclein propogation, using pre-formed fibril injection, we observed that loss of perivascular AQP4 localization increased α-synuclein aggregates. Our results indicate α-synuclein clearance and propagation are mediated by glymphatic function and that AQP4 mis-localization observed in the presence of human synucleinopathy may contribute to the development and propagation of Lewy body pathology in conditions such as Lewy Body Dementia and Parkinson's disease.
Related Topics
Concepts
Glymphatic system
Dementia with Lewy bodies
Alpha-synuclein
Genetically modified mouse
Synucleinopathies
Pathology
Neuroscience
Lewy body
Parkinson's disease
Transgene
Biology
Medicine
Dementia
Cerebrospinal fluid
Disease
Gene
Biochemistry
Metadata
- Type
- preprint
- Language
- en
- Landing Page
- https://doi.org/10.1101/2024.08.14.607971
- https://www.biorxiv.org/content/biorxiv/early/2024/08/19/2024.08.14.607971.full.pdf
- OA Status
- green
- Cited By
- 6
- References
- 73
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W4401696429
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W4401696429Canonical identifier for this work in OpenAlex
- DOI
-
https://doi.org/10.1101/2024.08.14.607971Digital Object Identifier
- Title
-
Aquaporin-4 mis-localization slows glymphatic clearance of α-synuclein and promotes α-synuclein pathology and aggregate propagationWork title
- Type
-
preprintOpenAlex work type
- Language
-
enPrimary language
- Publication year
-
2024Year of publication
- Publication date
-
2024-08-19Full publication date if available
- Authors
-
Molly Braun, Matthew Simon, Jay Jang, Keith Sanderson, J Swierz, Mathew Sevao, Alexandra Pincus, Allison J. Schaser, Jonathan E. Elliott, Miranda M. Lim, Vivek K. Unni, Abigail G. Schindler, C. Dirk Keene, Caitlin S. Latimer, Jeffrey J. IliffList of authors in order
- Landing page
-
https://doi.org/10.1101/2024.08.14.607971Publisher landing page
- PDF URL
-
https://www.biorxiv.org/content/biorxiv/early/2024/08/19/2024.08.14.607971.full.pdfDirect link to full text PDF
- Open access
-
YesWhether a free full text is available
- OA status
-
greenOpen access status per OpenAlex
- OA URL
-
https://www.biorxiv.org/content/biorxiv/early/2024/08/19/2024.08.14.607971.full.pdfDirect OA link when available
- Concepts
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Glymphatic system, Dementia with Lewy bodies, Alpha-synuclein, Genetically modified mouse, Synucleinopathies, Pathology, Neuroscience, Lewy body, Parkinson's disease, Transgene, Biology, Medicine, Dementia, Cerebrospinal fluid, Disease, Gene, BiochemistryTop concepts (fields/topics) attached by OpenAlex
- Cited by
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6Total citation count in OpenAlex
- Citations by year (recent)
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2025: 6Per-year citation counts (last 5 years)
- References (count)
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73Number of works referenced by this work
- Related works (count)
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10Other works algorithmically related by OpenAlex
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