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Endosomal recycling reconciles the Alzheimer's disease paradox
Abstract
A hub-and-spoke model with endosomal recycling as the hub can reconcile the pathogenic contribution of amyloid precursor protein to Alzheimer’s disease.
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Documenting that neuronal pathologies were resistant to knocking out tau supports the hypothesis that AD's neuronal and microglia pathology might occur independent of, and in parallel to, tau pathology.
“Furthermore, documenting that the neuronal pathologies were resistant to knocking out tau supports the hypothesis that AD’s neuronal and microglia pathology might occur independent of, and in parallel to, tau pathology (Small and Petsko, 2020).”
From The neuronal retromer can regulate both neuronal and microglial phenotypes of Alzheimer's disease (2022) · cites this paper as Small and Petsko, 2020
Retromer defects in sporadic Alzheimer's disease can occur independent of, and upstream to, either amyloid or tau pathology.
“recent studies suggest that retromer defects in sporadic AD can occur independent of, and upstream, to either amyloid or tau pathology (Small and Petsko, 2020).”
From The neuronal retromer can regulate both neuronal and microglial phenotypes of Alzheimer's disease (2022) · cites this paper as Small and Petsko, 2020
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Research works printed but not linked: 9
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- 10.1016/j.celrep.2020.107719 · DOI · Paper page
- 10.1016/j.neuron.2019.07.010 · DOI
- 10.1038/s41380-019-0364-x · DOI
- 10.1016/j.stemcr.2018.01.031 · DOI · Paper page
- 10.1016/j.neuron.2017.03.020 · DOI · Paper page
- 10.1038/s41418-019-0487-2 · DOI · Paper page
- 10.1126/scitranslmed.aba6334 · DOI · Paper page
- 10.1523/JNEUROSCI.3621-17.2018 · DOI
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Knopman, D. S., Amieva, H., Petersen, R. C., Chételat, G., Holtzman, D. M., Hyman, B. T., Nixon, R. A., & Jones, D. T. (2021) · Nature Reviews Disease Primers · doi:10.1038/s41572-021-00269-y · Cited by 2,606
Clinical diagnosis of Alzheimer’s disease: Recommendations of the International Working Group
Dubois, B., Villain, N., Frisoni, G. B., Rabinovici, G. D., Sabbagh, M., Cappa, S., Bejanin, A., Bombois, S., Epelbaum, S., Teichmann, M., et al. (2021) · The Lancet Neurology · doi:10.1016/s1474-4422(21)00066-1 · Cited by 1,051
“Besides the dominating amyloid cascade model, additional pathogenesis models have been advanced, including the role of endosomal recycling deficiency 21 , of immunity, of lipid metabolism and endocytosis deficiency 22 , of vascular dysfunction 23 , etc.”
BackgroundThe neuronal retromer can regulate both neuronal and microglial phenotypes of Alzheimer's disease
Qureshi, Y. H., Berman, D. E., Marsh, S. E., Klein, R. L., Patel, V. M., Simoes, S., Kannan, S., Petsko, G. A., Stevens, B., & Small, S. A. (2022) · Cell Reports · doi:10.1016/j.celrep.2021.110262 · Cited by 31
Self-citationRamonet, D., Daerr, A., & Hallbeck, M. (2025) · Acta Neuropathologica Communications · doi:10.1186/s40478-025-02096-8 · Cited by 7
Protective ApoE variants support neuronal function by extracting peroxidated lipids
Ralhan, I., Do, A. D., Bae, J.-Y., Feringa, F. M., Cai, W., Chang, J., Chik, K., Lee, N. Y., Gerry, C., van der Kant, R., et al. (2025) · bioRxiv · doi:10.1101/2025.03.05.641722 · Cited by 4
Metadata
- Authors
- Small, S. A., & Petsko, G. A.
- Affiliations
- Alzheimer’s Disease Research Center, Department of Neurology, Columbia University, New York, NY 10032, USA.
- Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA 02115, USA.
- Venue
- Science Translational Medicine
- Published
- 2020-12-02
- Volume
- 12
- Issue
- 572
- ISSN
- 1946-6234
- 1946-6242
- PMC
- PMC8025181
- Cited by
- 60
- References
- 0
- Language
- en
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