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Trans. R. Soc. B"],"published-print":{"date-parts":[[2024,4,8]]},"abstract":"<jats:p>\n                    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.\n                    <jats:italic>BIN1<\/jats:italic>\n                    and\n                    <jats:italic>PICALM<\/jats:italic>\n                    are two of the most significant late-onset AD risk genes after\n                    <jats:italic>APOE<\/jats:italic>\n                    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\u2014phagocytosis\u2014for 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.\n                  <\/jats:p>\n                  <jats:p>This article is part of a discussion meeting issue \u2018Understanding the endo-lysosomal network in neurodegeneration\u2019.<\/jats:p>","DOI":"10.1098\/rstb.2022.0378","type":"journal-article","created":{"date-parts":[[2024,2,18]],"date-time":"2024-02-18T19:05:18Z","timestamp":1708283118000},"update-policy":"https:\/\/doi.org\/10.1098\/crossmark-policy","source":"Crossref","is-referenced-by-count":20,"title":["Cell type-specific functions of Alzheimer's disease endocytic risk genes"],"prefix":"10.1098","volume":"379","author":[{"given":"Johanna-Katharina","family":"Maninger","sequence":"first","affiliation":[{"name":"Cardiff University, Dementia Research Institute, Cardiff University\u00b8 Cardiff, CF24 4HQ, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Karolina","family":"Nowak","sequence":"additional","affiliation":[{"name":"Cardiff University, Dementia Research Institute, Cardiff University\u00b8 Cardiff, CF24 4HQ, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Srilakshmi","family":"Goberdhan","sequence":"additional","affiliation":[{"name":"Cardiff University, Dementia Research Institute, Cardiff University\u00b8 Cardiff, CF24 4HQ, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rachel","family":"O'Donoghue","sequence":"additional","affiliation":[{"name":"Cardiff University, Dementia Research Institute, Cardiff University\u00b8 Cardiff, CF24 4HQ, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8350-6928","authenticated-orcid":true,"given":"Natalie","family":"Connor-Robson","sequence":"additional","affiliation":[{"name":"Cardiff University, Dementia Research Institute, Cardiff University\u00b8 Cardiff, CF24 4HQ, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"175","published-online":{"date-parts":[[2024,2,19]]},"reference":[{"key":"e_1_3_7_2_2","unstructured":"Alzheimer\u2019s Research UK. 2020 Dementia Statistics Hub. 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