APOE genotype regulates pathology and disease progression in synucleinopathy
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APOE genotype regulates disease development in mouse models of α-synucleinopathy and affects cognition in patients with Parkinson’s disease.
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APOEε4 has been associated with a faster rate of cognitive decline in people with Parkinson disease, independent of Alzheimer disease neuropathology assessed by levels of CSF biomarkers Aβ42 and pTau.
“APOEε4 has been associated with a faster rate of cognitive decline in people with Parkinson disease, independent of AD neuropathology assessed by levels of CSF biomarkers Aβ42 and pTau69.”
From Multifaceted roles of APOE in Alzheimer disease (2024) · cites this paper as [69]
The APOE2 mice have improved motor function and prolonged survival compared with APOE3-expressing mice, suggesting that the effect of APOE on α-synucleinopathies is independent of its effect on Aβ.
“Furthermore, the APOE2 mice have improved motor function and prolonged survival compared with APOE3-expressing mice, suggesting that the effect of APOE on α-synucleinopathies is independent of its effect on Aβ69.”
From Multifaceted roles of APOE in Alzheimer disease (2024) · cites this paper as [69]
Studies using APOE-targeted replacement mice crossed with mutant α-synuclein mice have reported that APOE4 mice have increased aggregation of α-synuclein, whereas APOE2 mice have very limited α-synuclein aggregates.
“Studies using APOE-targeted replacement (APOE-TR) mice crossed with mutant α-synuclein (αSyn) mice have reported that APOE4 mice have increased aggregation of αSyn, whereas APOE2 mice have very limited αSyn aggregates.”
From Multifaceted roles of APOE in Alzheimer disease (2024) · cites this paper as [69]
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Cites
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Self-citationApoE4 markedly exacerbates tau-mediated neurodegeneration in a mouse model of tauopathy
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Self-citationHuman<i>APOE</i>Isoform-Dependent Effects on Brain β-Amyloid Levels in PDAPP Transgenic Mice
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Extracellular α-synuclein levels are regulated by neuronal activity
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Apolipoprotein E mediation of neuro-inflammation in a murine model of multiple sclerosis
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- Authors
- Davis, A. A., Inman, C. E., Wargel, Z. M., Dube, U., Freeberg, B. M., Galluppi, A., Haines, J. N., Dhavale, D. D., Miller, R., Choudhury, F. A., Sullivan, P. M., Cruchaga, C., Perlmutter, J. S., Ulrich, J. D., Benitez, B. A., Kotzbauer, P. T., & Holtzman, D. M.
- Affiliations
- Washington University in St. Louis (US)
- Duke Medical Center (US)
- Hope Center for Neurologic Disease, Washington University, St. Louis, MO 63110, USA.
- Corresponding author
- Davis, Albert A.
- Holtzman, David M.
- ORCID
- Venue
- Science Translational Medicine
- Published
- 2020-02-05
- Volume
- 12
- Issue
- 529
- Pages
- eaay3069
- ISSN
- 1946-6234 (ISSN-L)
- 1946-6242
- PMC
- PMC7289511
- OpenAlex
- W3004888206
- Cited by
- 177
- References
- 12
- Citations by year
- 2026: 19 · 2025: 33 · 2024: 29 · 2023: 24 · 2022: 31 · 2021: 23 · 2020: 18
- FWCI
- 10.33
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science Translational Medicine (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- HAL (submittedVersion)
- Funders
- National Institutes of Health (K08NS101118, R01AG044546, RF1AG053303, RF1AG058501, U01AG052411, U01AG058922, NS097799, R01NS090934, R01AG047644, NS075321)
- the JPB Foundation
- American Brain Foundation
- American Academy of Neurology
- BrightFocus Foundation
- Mary E. Groff Surgical and Medical Research and Education Charitable Trust
- Dobbins Family Fund
- Barnes-Jewish Hospital Foundation
- The Riney Foundation
- The American Parkinson Disease Association
- The Greater St. Louis Chapter of the APDA
- Topics
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
- Keywords
- APOE genotype, synucleinopathies, Parkinson's disease, mouse model, disease progression, cognitive function, neurodegeneration
- MeSH terms
- Synucleinopathies, Animals, Apolipoproteins E, Genotype, Humans, Disease Progression, Mice, Apolipoprotein E4
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