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However, it is not fully understood how these compound proteinopathies are interconnected. Here, we show that transplantation of amyloid-\u03b2 oligomer-activated microglia into the striatum of na\u00efve mice was sufficient to generate all the features of Alzheimer\u2019s disease, including widespread tauopathy and synucleinopathy, gliosis, neuroinflammation, synapse loss, neuronal death, and cognitive and motor deficits. These pathological features were eliminated by microglia depletion and anti-inflammatory drug administration.<\/jats:p>\n                  <jats:p>Our results suggest the crucial roles of microglia-driven inflammation in development of mixed pathology. This study provides not only mechanistic insights into amyloid-\u03b2 oligomer-triggered proteinopathies but also a novel animal model recapitulating the salient features of Alzheimer\u2019s disease.<\/jats:p>","DOI":"10.1093\/brain\/awae221","type":"journal-article","created":{"date-parts":[[2024,7,8]],"date-time":"2024-07-08T08:31:55Z","timestamp":1720427515000},"page":"4105-4120","source":"Crossref","is-referenced-by-count":13,"title":["Amyloid-\u03b2-activated microglia can induce compound proteinopathies"],"prefix":"10.1093","volume":"147","author":[{"given":"Sang Hwan","family":"Lee","sequence":"first","affiliation":[{"name":"Department of Biomedical Sciences, Seoul National University College of Medicine , Seoul 03080 ,","place":["Korea"]},{"name":"Neuroscience Research Institute, Medical Research Center, Seoul National University , Seoul 03080 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