Wolfdieter Springer

This study shows that PINK1 loss in astrocytes causes inflammation and neuronal death through non-cell-autonomous mechanisms, and that autophagy enhancement can reverse these effects.

This study identifies phosphorylated ubiquitin (pS65Ub) as a signaling molecule that mediates mitochondrial-to-nuclear communication by modulating histone ubiquitination and gene expression in Parkinson's disease.

This study profiles mitochondrial respiration in IBM muscle tissue, identifying sex-specific impairments in respiration and OXPHOS complexes, along with correlations with disease severity.

This study shows that reducing mitochondrial complex I activity in mice induces AD-like transcriptomic changes, which are partially reversed by a complex I inhibitor.

This study shows LRRK2 and PINK1 function in parallel neuroprotective pathways affecting ciliogenesis in Parkinson's disease, suggesting shared therapeutic targets.

This study examines PINK1-PRKN signaling in mice during aging, showing increased gene expression and enzymatic activity in multiple tissues, with the heart showing the most pronounced activation.

This study shows that Rag-GTPases regulate B cell metabolism and immunity by restraining TFEB/TFE3 to maintain mitochondrial fitness and support T-independent humoral immunity.

This paper develops and characterizes novel phospho-ubiquitin antibodies to detect low levels of p-S65-Ub, a marker of mitochondrial damage, in cells and tissues.

This study investigates changes in the UFMylation pathway in Alzheimer's disease brains, finding increased UFM1 conjugation and associations with pathological tau.

The paper identifies miR-29 and ATG9A as regulators of mitophagy and discovers EOPD-linked variants in ATG9A.

This study shows that alpha-synuclein oligomers reduce mitochondrial SIRT3 activity, impair mitochondrial dynamics, and that AICAR treatment restores SIRT3 and improves mitochondrial dysfunction in Parkinson's disease models.