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During normal aging, synapses decline, and \u03b2-amyloid (A\u03b2) accumulates intraneuronally. However, little is known about the underlying cell biological mechanisms. We studied neuronal aging using normal-aged brain and aged mouse primary neurons that accumulate lysosomal lipofuscin and show synapse loss. We identified the upregulation of amyloid precursor protein (APP) endocytosis as a neuronal aging mechanism that potentiates APP processing and A\u03b2 production in vitro and in vivo. The increased APP endocytosis may contribute to the early endosome enlargement observed in the aged brain. Mechanistically, we showed that clathrin-dependent APP endocytosis requires F-actin and that clathrin and endocytic F-actin increase with neuronal aging. Finally, A\u03b2 production inhibition reverts synaptic decline in aged neurons, whereas A\u03b2 accumulation, promoted by endocytosis upregulation in younger neurons, recapitulates aging-related synapse decline. Overall, we identify APP endocytosis upregulation as a potential mechanism of neuronal aging and, thus, a novel target to prevent late-onset Alzheimer's disease.<\/jats:p>\n                  <jats:p>This article has an associated First Person interview with the first author of the paper.<\/jats:p>","DOI":"10.1242\/jcs.255752","type":"journal-article","created":{"date-parts":[[2021,4,28]],"date-time":"2021-04-28T09:15:36Z","timestamp":1619601336000},"source":"Crossref","is-referenced-by-count":63,"title":["Upregulation of APP endocytosis by neuronal aging drives amyloid-dependent synapse loss"],"prefix":"10.1242","volume":"134","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0166-6552","authenticated-orcid":false,"given":"Tatiana","family":"Burrinha","sequence":"first","affiliation":[{"name":"iNOVA4Health, Chronic Diseases Research Center (CEDOC), NOVA Medical School (NMS), Universidade Nova de Lisboa, 1169-056 Lisboa, Portugal"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Isak","family":"Martinsson","sequence":"additional","affiliation":[{"name":"Experimental Dementia Research Unit, Lund University, 22184 Lund, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ricardo","family":"Gomes","sequence":"additional","affiliation":[{"name":"iNOVA4Health, Chronic Diseases Research Center (CEDOC), NOVA Medical School (NMS), Universidade Nova de Lisboa, 1169-056 Lisboa, Portugal"},{"name":"iBET - Instituto de Biologia Experimental e Tecnol\u00f3gica, Apartado 12, 2780-901 Oeiras, Portugal"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4369-6277","authenticated-orcid":false,"given":"Ana Paula","family":"Terrasso","sequence":"additional","affiliation":[{"name":"iNOVA4Health, Chronic Diseases Research Center (CEDOC), NOVA Medical School (NMS), Universidade Nova de Lisboa, 1169-056 Lisboa, Portugal"},{"name":"iBET - Instituto de Biologia Experimental e Tecnol\u00f3gica, Apartado 12, 2780-901 Oeiras, Portugal"},{"name":"Instituto de Tecnologia Qu\u00edmica e Biol\u00f3gica, Universidade Nova de Lisboa, Av. da Rep\u00fablica, 2780-157 Oeiras, Portugal"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5500-6325","authenticated-orcid":false,"given":"Gunnar K.","family":"Gouras","sequence":"additional","affiliation":[{"name":"Experimental Dementia Research Unit, Lund University, 22184 Lund, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9384-2896","authenticated-orcid":false,"given":"Cl\u00e1udia Guimas","family":"Almeida","sequence":"additional","affiliation":[{"name":"iNOVA4Health, Chronic Diseases Research Center (CEDOC), NOVA Medical School (NMS), Universidade Nova de Lisboa, 1169-056 Lisboa, Portugal"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"237","published-online":{"date-parts":[[2021,5,17]]},"reference":[{"key":"2022051110093817200_JCS255752C1","doi-asserted-by":"publisher","first-page":"8252","DOI":"10.1074\/jbc.M110.128512","article-title":"Copper promotes the trafficking of the amyloid precursor protein","volume":"286","author":"Acevedo","year":"2011","journal-title":"J. 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