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Stabilizing the Retromer Complex in a Human Stem Cell Model of Alzheimer’s Disease Reduces TAU Phosphorylation Independently of Amyloid Precursor Protein
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Stabilisation of Retromer expression is neuroprotective.
“with stabilisation of Retromer expression being neuroprotective [49][50][51][52].”
From Global identification of neuronal and astrocytic integral membrane proteins that require Retromer for their endosomal recycling (2026) · cites this paper as [51]
The Results report that stabilizing the retromer complex with R33 reduced Aβ and phosphorylated TAU in human stem-cell-derived neurons; the Discussion calls these effects potentially beneficial. The paper does not establish neuroprotection directly, and it tests stabilization of the complex rather than stabilization of retromer expression. (LLM, conf=0.84)
Experimental — accuracy not yet measuredSimilar co-regulation of Aβ and Tau through independent pathways has been shown for ApoE and the retromer complex.
“Similar co-regulation of Aβ and Tau through independent pathways have recently been shown for ApoE (Wang et al., 2018) and the retromer complex (Young et al., 2018).”
From Cholesterol Metabolism Is a Druggable Axis that Independently Regulates Tau and Amyloid-β in iPSC-Derived Alzheimer’s Disease Neurons (2019) · cites this paper as Young et al., 2018
Studies have provided proof-of-concept that retromer can be pharmacologically targeted.
“Notably, studies have already provided the proof-of-concept that retromer can be pharmacologically targeted (Young et al., 2018; Mecozzi et al., 2014)”
From The neuronal retromer can regulate both neuronal and microglial phenotypes of Alzheimer's disease (2022) · cites this paper as Young et al., 2018
Retromer stabilization has been suggested as a promising therapeutic approach to treat Alzheimer's disease, another retromer dysfunction-related disorder.
“Retromer stabilization has been suggested as a promising therapeutic approach to treat Alzheimer’s disease, another retromer dysfunction–related disorder;56,100”
From EHBP1 suppresses liver fibrosis in metabolic dysfunction-associated steatohepatitis (2025) · cites this paper as [56]
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Metadata
- Authors
- Young, J. E., Fong, L. K., Frankowski, H., Petsko, G. A., Small, S. A., & Goldstein, L. S. B.
- Venue
- Stem Cell Reports
- Publisher
- Elsevier BV
- Published
- 2018-03
- Volume
- 10
- Issue
- 3
- Pages
- 1046-1058
- ISSN
- 2213-6711
- PMC
- PMC5919412
- Cited by
- 110
- References
- 12
- Language
- en
- Licence
- Funders
- BrightFocus Foundation
- Alzheimer's Disease Research Center, Emory University
- University of Washington
- John H. Tietze Foundation Trust
- Ellison Medical Foundation
- National Institutes of Health (AG005136)
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