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Nevertheless, its cellular and molecular mechanisms remain incompletely understood, partially due to inadequate disease models. To illuminate early changes in AD, we developed a cerebrocortical organoid (CO) model with improved methodology. Our COs produce excitatory and inhibitory neurons alongside glia, utilizing established isogenic wild\u2010type and diseased human induced pluripotent stem cells (hiPSCs) carrying heterozygous familial AD mutations in PSEN1\n                    <jats:sup>\u0394E9<\/jats:sup>\n                    \/WT, PSEN1\n                    <jats:sup>M146V<\/jats:sup>\n                    \/WT, or APP\n                    <jats:sup>Swe<\/jats:sup>\n                    \/WT. In addition to amyloid\u2010beta (A\u03b2) accumulation, the AD COs display time\u2010progressive loss of monomeric Tau, and accumulation of aggregated high\u2010molecular\u2010weight (HMW) phospho(p)\u2010Tau species (pT181 and pT217). They also exhibit neuronal hyperexcitability reminiscent of early electroencephalography (EEG) clinical findings and synapse loss in AD patient brains. Single\u2010cell RNA\u2010sequencing analyses of AD and WT control COs reveal significant divergent molecular abnormalities in excitatory vs. inhibitory neurons, with several pathways being upregulated in one while downregulated in the other, providing insight into AD phenotypes. Finally, we show that chronic dosing with autophagy activators, including a novel mTOR inhibitor\u2010independent drug candidate, prevents pathologic A\u03b2 and HMW p\u2010Tau accumulation, normalizes hyperexcitability, and rescues synaptic loss in AD COs. Collectively, our results demonstrate this CO model as a useful platform for assessing early features of familial AD pathogenesis and for testing small\u2010molecule candidate therapeutics.\n                  <\/jats:p>","DOI":"10.1002\/advs.202514783","type":"journal-article","created":{"date-parts":[[2026,1,27]],"date-time":"2026-01-27T15:58:12Z","timestamp":1769529492000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Autophagy Activators Normalize Aberrant Tau Proteostasis and Rescue Synapses in Human Familial Alzheimer's Disease iPSC\u2010Derived Cortical Organoids"],"prefix":"10.1002","volume":"13","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4072-1131","authenticated-orcid":false,"given":"Sergio R.","family":"Labra","sequence":"first","affiliation":[{"name":"Neurodegeneration New Medicines Center The Scripps Research Institute  La Jolla California USA"},{"name":"Department of Molecular and Cellular 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