<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Lind-Holm Mogensen F</submitter><funding>Fonds National de la Recherche Luxembourg</funding><pagination>174</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11253405</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>21(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Specific microglia responses are thought to contribute to the development and progression of neurodegenerative diseases, including Parkinson's disease (PD). However, the phenotypic acquisition of microglial cells and their role during the underlying neuroinflammatory processes remain largely elusive. Here, according to the multiple-hit hypothesis, which stipulates that PD etiology is determined by a combination of genetics and various environmental risk factors, we investigate microglial transcriptional programs and morphological adaptations under PARK7/DJ-1 deficiency, a genetic cause of PD, during lipopolysaccharide (LPS)-induced inflammation.&lt;h4>Methods&lt;/h4>Using a combination of single-cell RNA-sequencing, bulk RNA-sequencing, multicolor flow cytometry and immunofluo</pubmed_abstract><journal>Journal of neuroinflammation</journal><pubmed_title>PARK7/DJ-1 deficiency impairs microglial activation in response to LPS-induced inflammation.</pubmed_title><pmcid>PMC11253405</pmcid><funding_grant_id>C19/BM/13688526</funding_grant_id><funding_grant_id>FNR9631103</funding_grant_id><funding_grant_id>AFR/6916713</funding_grant_id><funding_grant_id>PRIDE21/16749720</funding_grant_id><funding_grant_id>PRIDE/14254520/I2TRON</funding_grant_id><funding_grant_id>C21/BM/15739125/DIOMEDES</funding_grant_id><funding_grant_id>INTER/DFG/17/11583046</funding_grant_id><funding_grant_id>PRIDE/10907093/CRITICS</funding_grant_id><pubmed_authors>Antony PMA</pubmed_authors><pubmed_authors>Nicot N</pubmed_authors><pubmed_authors>Poovathingal SK</pubmed_authors><pubmed_authors>Tziortziou M</pubmed_authors><pubmed_authors>Pereira SL</pubmed_authors><pubmed_authors>Skupin A</pubmed_authors><pubmed_authors>Kaoma T</pubmed_authors><pubmed_authors>Badanjak K</pubmed_authors><pubmed_authors>Wurst W</pubmed_authors><pubmed_authors>Michelucci A</pubmed_authors><pubmed_authors>Ameli C</pubmed_authors><pubmed_authors>Coowar D</pubmed_authors><pubmed_authors>Poli A</pubmed_authors><pubmed_authors>Nazarov PV</pubmed_authors><pubmed_authors>Lind-Holm Mogensen F</pubmed_authors><pubmed_authors>Ginolhac A</pubmed_authors><pubmed_authors>Muller A</pubmed_authors><pubmed_authors>Vogt Weisenhorn DM</pubmed_authors><pubmed_authors>Grunewald A</pubmed_authors><pubmed_authors>Sousa C</pubmed_authors><pubmed_authors>Scafidi A</pubmed_authors></additional><is_claimable>false</is_claimable><name>PARK7/DJ-1 deficiency impairs microglial activation in response to LPS-induced inflammation.</name><description>&lt;h4>Background&lt;/h4>Specific microglia responses are thought to contribute to the development and progression of neurodegenerative diseases, including Parkinson's disease (PD). However, the phenotypic acquisition of microglial cells and their role during the underlying neuroinflammatory processes remain largely elusive. Here, according to the multiple-hit hypothesis, which stipulates that PD etiology is determined by a combination of genetics and various environmental risk factors, we investigate microglial transcriptional programs and morphological adaptations under PARK7/DJ-1 deficiency, a genetic cause of PD, during lipopolysaccharide (LPS)-induced inflammation.&lt;h4>Methods&lt;/h4>Using a combination of single-cell RNA-sequencing, bulk RNA-sequencing, multicolor flow cytometry and immunofluo</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Jul</publication><modification>2025-04-04T15:02:36.848Z</modification><creation>2025-04-04T15:02:36.848Z</creation></dates><accession>S-EPMC11253405</accession><cross_references><pubmed>39014482</pubmed><doi>10.1186/s12974-024-03164-x</doi></cross_references></HashMap>