Stephan A. Müller

This study shows that DJ-1 deficiency impairs VMAT2 function and vesicle dynamics, leading to dopamine oxidation and α-synuclein pathology in Parkinson's disease neurons.

This study investigates how TREM2 expression levels affect microglial function, metabolism, and response to TREM2 agonists in a mouse model of Alzheimer's disease.

This paper develops a 3D cortical brain tissue model with mature microglia that recapitulates Alzheimer's disease hallmarks and enables study of microglia phenotypes.

This study investigates BACE1's role in sleep-wake cycles through enzymatic and non-enzymatic actions using mouse models, finding altered sleep patterns and EEG characteristics in mutants.

This study shows that DJ-1 mutations impair astrocytic dopamine metabolism, leading to disrupted detoxification and potential contribution to Parkinson's disease pathogenesis.

The paper uses iPSC-derived microglia from BPAN patients to identify immune-related alterations and immunomodulatory signaling changes, revealing a shift to a reactive, disease-associated state.

This study shows that long-term anti-Aβ treatment reduces amyloid plaques and microglial activation but leaves residual plaques with persistent immune activity.

This study identifies iRhom2 as a modifier of ADAM17-mediated TREM2 proteolysis in microglia, linking it to Alzheimer's disease risk.

This study shows that loss of CLN3 in microglia causes lipid metabolism defects and impaired myelin turnover, leading to early neuroinflammation in a mouse model of CLN3 disease.

This study shows that the PLCgamma2-P522R variant reduces beta-amyloid pathology and enhances microglial function in AD models, suggesting an anti-ageing mechanism.

The paper introduces an improved method for collecting and analyzing murine cerebrospinal fluid, enabling quantitative proteomics and revealing proteome changes in Alzheimer's disease models.

The paper identifies cellular sources of PET signals in glioblastoma by combining radiotracer uptake with 3D-histology and proteomics, showing tumor cells mainly contribute to TSPO enrichment while TAMs have specific PET targets.

The paper identifies a microglial activity biomarker panel that differentiates FTD-GRN and AD cases from controls using proteomic analysis in mouse models and human samples.

This study shows endogenous retroviruses enhance prion-like spreading of protein aggregates between cells, suggesting antiviral drugs could inhibit disease progression.

The paper shows that TCA cycle dysfunction contributes to axonal energy deficiency in neuroinflammatory lesions and that restoring TCA enzymes can alleviate this deficit.

This study identifies RUS, a lncRNA that promotes neurogenesis by regulating gene expression and epigenetic interactions during neuronal differentiation.

The paper shows viral ligand-receptor interactions enhance the spread of protein misfolding via extracellular vesicles and direct cell contact.

This study shows that loss of NPC1 in microglia increases phagocytic uptake and impairs lipid trafficking, leading to myelin accumulation and potential therapeutic implications.

The paper develops a method to analyze the secretome of mouse brain cells and identifies cell type-specific secreted proteins, revealing proteolytic cleavage of membrane proteins.

This study identifies proteomic changes in microglia during Alzheimer's disease progression in mouse models, showing fibrillar Aβ drives microglial dysfunction.