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It is also characterized by abnormal inclusion vesicles, termed Lewy bodies (LBs), enriched with \u03b1-synuclein aggregates that may induce inflammation and neurotoxicity. The possibility that factors involved in other neurodegenerative diseases also affect PD-related pathologies, such as \u03b1-synuclein uptake, was examined. The\n                    <jats:italic>apoe4<\/jats:italic>\n                    allele is a major genetic risk factor for Alzheimer\u2019s disease (AD) and has also been suggested to be involved in PD. Here, we examined the effects of APOE isoform expression on \u03b1-synuclein uptake and autophagy in astrocytes expressing the\n                    <jats:italic>apoe3<\/jats:italic>\n                    or\n                    <jats:italic>apoe4<\/jats:italic>\n                    alleles. Using multiple autophagy manipulations (EBSS, chloroquine, and rapamycin treatments), we found that \u03b1-synuclein uptake and autophagy readouts differ between\n                    <jats:italic>APOE3<\/jats:italic>\n                    and\n                    <jats:italic>APOE4<\/jats:italic>\n                    astrocytes, supporting a functional link between autophagy status and \u03b1-synuclein levels. Astrocytes expressing\n                    <jats:italic>APOE4<\/jats:italic>\n                    exhibit reduced uptake of \u03b1-synuclein and reduced autophagy. Moreover, \u03b1-synuclein treatment inhibits autophagy mainly in\n                    <jats:italic>APOE3<\/jats:italic>\n                    -expressing cells. Additional experiments showed that the autophagy inhibitor chloroquine reduced \u03b1-synuclein uptake in\n                    <jats:italic>APOE3<\/jats:italic>\n                    astrocytes but not in\n                    <jats:italic>APOE4<\/jats:italic>\n                    astrocytes, while\u00a0the autophagy enhancer rapamycin increased \u03b1-synuclein uptake in\n                    <jats:italic>APOE4<\/jats:italic>\n                    -expressing astrocytes. In addition, we found that Toll-like receptor 2 (TLR2) levels are elevated at both the mRNA and protein levels in\n                    <jats:italic>APOE4<\/jats:italic>\n                    -expressing astrocytes, whereas \u03b1-synuclein increased only TLR2 mRNA levels in\n                    <jats:italic>APOE3<\/jats:italic>\n                    -expressing astrocytes. Using the neurotoxin 1-methyl-4-phenylpyridinium (MPP\n                    <jats:sup>+<\/jats:sup>\n                    ), we found that it affects cell growth in both\n                    <jats:italic>APOE3<\/jats:italic>\n                    and\n                    <jats:italic>APOE4<\/jats:italic>\n                    -expressing astrocytes. MPP\n                    <jats:sup>+<\/jats:sup>\n                    treatment also reduced autophagy which was partially corrected by rapamycin. Taken together, these findings show that in astrocytes,\n                    <jats:italic>APOE4<\/jats:italic>\n                    impairs \u03b1-synuclein uptake, which was emended by rapamycin and \u03b1-synuclein inhibits autophagy mainly in\n                    <jats:italic>APOE3<\/jats:italic>\n                    . These findings suggest that autophagy-targeting strategies can modulate astrocyte \u03b1-synuclein uptake; however, given the observed reductions in astrocyte cell number following rapamycin treatment, further optimization or examination of alternative autophagy modulators is needed.\n                  <\/jats:p>","DOI":"10.1007\/s12035-026-05996-5","type":"journal-article","created":{"date-parts":[[2026,6,11]],"date-time":"2026-06-11T05:35:58Z","timestamp":1781156158000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["APOE4-Expressing Astrocytes Exhibit Parkinson\u2019s Disease\u2013Related Pathology"],"prefix":"10.1007","volume":"63","author":[{"given":"Lior","family":"Nechushtai","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anna","family":"Popov","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Roni","family":"Haklai","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel M.","family":"Michaelson","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dan","family":"Frenkel","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ronit","family":"Pinkas-Kramarski","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,6,11]]},"reference":[{"key":"5996_CR1","doi-asserted-by":"publisher","unstructured":"Masato A, Plotegher N, Boassa D, Bubacco L (2019) Impaired dopamine metabolism in Parkinson\u2019s disease pathogenesis. 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