PARK7/DJ-1 deficiency modulates microglial activation in response to LPS-induced inflammation

Specific microglia responses are thought to contribute to the development and progression of various neurodegenerative diseases, including Parkinson’s disease (PD). However, the phenotypic acquisition of microglial cells and their role during the underlying neuroinflammatory processes remain largely obscure. 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.

Type: Transcriptome Analysis
Archiver: European Genome-Phenome Archive (EGA)

1 Dataset 1 Publication

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Dataset ID	Description	Technology	Samples
EGAD50000000291	Starting point is one patient from which iPSC cells are created, some received a genome correction to be called iCtrl from those two batches (DJ1 and iCtrl). 3 independent differentiation to Microglia cells were done, named R1, R2 and R3. On top, growing conditions were either untreated or LPS, leading to the 12 samples.	NextSeq 500	12

Publications	Citations
PARK7/DJ-1 deficiency impairs microglial activation in response to LPS-induced inflammation. Lind-Holm Mogensen F, Sousa C, Ameli C, Badanjak K, Pereira SL, Muller A, Kaoma T, Coowar D, Scafidi A, Poovathingal SK, Tziortziou M, Antony PMA, Nicot N, Ginolhac A, Vogt Weisenhorn DM, Wurst W, Poli A, Nazarov PV, Skupin A, Grünewald A, Michelucci A. J Neuroinflammation 21: 2024 174	2