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Cell type-specific functions of Alzheimer's disease endocytic risk genes
Abstract
Endocytosis is a key cellular pathway required for the internalization of cellular nutrients, lipids and receptor-bound cargoes. It is also critical for the recycling of cellular components, cellular trafficking and membrane dynamics. The endocytic pathway has been consistently implicated in Alzheimer's disease (AD) through repeated genome-wide association studies and the existence of rare coding mutations in endocytic genes. BIN1 and PICALM are two of the most significant late-onset AD risk genes after APOE and are both key to clathrin-mediated endocytic biology. Pathological studies also demonstrate that endocytic dysfunction is an early characteristic of late-onset AD, being seen in the prodromal phase of the disease. Different cell types of the brain have specific requirements of the endocytic pathway. Neurons require efficient recycling of synaptic vesicles and microglia use the specialized form of endocytosis—phagocytosis—for their normal function. Therefore, disease-associated changes in endocytic genes will have varied impacts across different cell types, which remains to be fully explored. Given the genetic and pathological evidence for endocytic dysfunction in AD, understanding how such changes and the related cell type-specific vulnerabilities impact normal cellular function and contribute to disease is vital and could present novel therapeutic opportunities. This article is part of a discussion meeting issue ‘Understanding the endo-lysosomal network in neurodegeneration’.
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Identification of AD risk genes highly expressed in microglia by GWAS supports the idea that dysfunctional microglia may contribute to onset and/or progression of AD.
“Identification of ad risk genes highly expressed in microglia by genome‐wide association studies (GWAS) further supports the idea that dysfunctional microglia may contribute to onset and/or progression of ad (Maninger et al. 2024; McQuade and Blurton‐Jones 2019).”
From The Alzheimer's Disease Gene SORL1 Regulates Lysosome Function in Human Microglia (2025) · cites this paper as Maninger et al. 2024
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Cited by
Sorted by citations
The Alzheimer's Disease Gene SORL1 Regulates Lysosome Function in Human Microglia
Mishra, S., Morshed, N., Sidhu, S. B., Kinoshita, C., Stevens, B., Jayadev, S., & Young, J. E. (2025) · Glia · doi:10.1002/glia.70009 · Cited by 31
Jaye, S., Sandau, U. S., & Saugstad, J. A. (2024) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2024.1378576 · Cited by 26
Endosomal protein DENND10 promotes developmental competence of neurite extension
Li, A., Zhang, J., Ma, C., Qi, L., Hu, Q., Li, Q., Fang, Y., Song, J., Liu, Y., & Zhang, Y. (2025) · iScience · doi:10.1016/j.isci.2025.112385
Metadata
- Authors
- Maninger, J.-K., Nowak, K., Goberdhan, S., O'Donoghue, R., & Connor-Robson, N.
- Affiliations
- Cardiff University, Dementia Research Institute, Cardiff University¸ Cardiff, CF24 4HQ, UK
- Venue
- Philosophical Transactions of the Royal Society B: Biological Sciences
- Publisher
- The Royal Society
- Published
- 2024-02-19
- Volume
- 379
- Issue
- 1899
- ISSN
- 0962-8436
- 1471-2970
- PMC
- PMC10874703
- Cited by
- 22
- References
- 43
- Language
- en
- Funders
- UK Dementia Research Institute (DRI-PP2021-06, UK DRI-DSI2020-IPMAR)
- Alzheimer's Society (AS-PhD-21-011)
- BRACE (BR2222)
- Alzheimer's Research UK (ARUK-RF2020A-004)
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