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In Parkinson's disease (PD), dopaminergic terminals degenerate in the striatum, leading to dopamine depletion, which in turn causes alterations in the basal ganglia circuits that are essential for movement control. However, the reasons for dopaminergic neuron terminal degeneration in the striatum are still not understood. The\n                      <jats:italic>LRRK2<\/jats:italic>\n                      gene is highly expressed in the striatum, and the LRRK2\u2010G2019S mutation is one of the most common mutations associated with PD. It is therefore tempting to speculate that dysregulations in the striatal functionality can initiate or contribute to the dopaminergic neuron terminals' degeneration.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>We aimed to examine the phenotypic differences between healthy and patient striatum organoids carrying the LRRK2\u2010G2019S mutation to assess whether specific alterations in the striatum that are independent of dopaminergic input could contribute to the development of the disease.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Striatum organoids were generated using healthy and PD patient\u2013induced pluripotent stem cell lines, and they were cultured until day 80. We evaluated the levels of striatum\u2010specific proteins, and we performed proteomics and kinase activity analysis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>PD striatum organoids revealed increased abundance of DRD2, DARPP32, and CDK5. Proteomics and kinase activity analysis demonstrated an inflammatory phenotype, which was further validated by investigating the occurrence of reactive astrocytes.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      Striatum organoids recapitulate PD\u2010relevant phenotypes autonomously, independent of dopaminergic input. This includes a significant inflammatory phenotype. \u00a9 2026 The Author(s).\n                      <jats:italic>Movement Disorders<\/jats:italic>\n                      published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/mds.70176","type":"journal-article","created":{"date-parts":[[2026,2,11]],"date-time":"2026-02-11T12:13:01Z","timestamp":1770811981000},"page":"948-961","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Parkinson's Disease Patient\u2010Specific Striatum Organoids Show Hallmarks of Increased Inflammation"],"prefix":"10.1002","volume":"41","author":[{"given":"Kyriaki","family":"Barmpa","sequence":"first","affiliation":[{"name":"Developmental and Cellular Biology, Luxembourg Centre for Systems Biomedicine University of Luxembourg  Esch\u2010sur\u2010Alzette 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