A5033612849- Mitochondrial Function and Pathology
- Neurogenesis and neuroplasticity mechanisms
- Neuroinflammation and Neurodegeneration Mechanisms
- Microtubule and mitosis dynamics
- Neuroscience and Neuropharmacology Research
- Anesthesia and Neurotoxicity Research
- Cancer, Stress, Anesthesia, and Immune Response
- Single-cell and spatial transcriptomics
- Alzheimer's disease research and treatments
- Redox biology and oxidative stress
- Traumatic Brain Injury and Neurovascular Disturbances
- Cancer Cells and Metastasis
- Virus-based gene therapy research
- RNA Interference and Gene Delivery
- Neuroscience and Neural Engineering
- Lung Cancer Research Studies
Ludwig-Maximilians-Universität München
2024-2025
Helmholtz Zentrum München
2024-2025
University of Cologne
2018-2024
Cologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases
2018-2024
The transition between quiescence and activation in neural stem progenitor cells (NSPCs) is coupled with reversible changes energy metabolism key implications for lifelong NSPC self-renewal neurogenesis. How this metabolic plasticity ensured activity states unclear. We find that a state-specific rewiring of the mitochondrial proteome by i-AAA peptidase YME1L required to preserve self-renewal. controls abundance numerous substrates quiescent NSPCs, its deletion activates differentiation...
Integration of new neurons into adult hippocampal circuits is a process coordinated by local and long-range synaptic inputs. To achieve stable integration uniquely contribute to function, immature are endowed with critical period heightened plasticity, yet it remains unclear which mechanisms sustain this form plasticity during neuronal maturation. We found that as enter their period, transient surge in fusion dynamics stabilizes elongated mitochondrial morphologies dendrites fuel plasticity....
Research Article2 November 2018Open Access Source DataTransparent process Loss of the mitochondrial i-AAA protease YME1L leads to ocular dysfunction and spinal axonopathy Hans-Georg Sprenger Max-Planck-Institute for Biology Ageing, Cologne, Germany Institute Genetics Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University Search more papers by this author Gulzar Wani Annika Hesseling Tim König Maria Patron Thomas MacVicar Sofia Ahola Timothy...
Abstract Astrocyte heterogeneity has been well explored, but our understanding of white matter (WM) astrocytes and their distinctions from gray (GM) remains limited. Here, we compared cortical GM WM/corpus callosum (WM/CC) using single-cell RNA sequencing spatial transcriptomics the murine forebrain. The comparison revealed similarities also significant differences between WM astrocytes, including cytoskeletal metabolic hallmarks specific to with molecular properties shared human astrocytes....
Abstract Small cell lung cancer (SCLC) is a highly aggressive type of cancer, characterized by rapid proliferation, early metastatic spread, clinical recurrence and high rate mortality. Using in vivo insertional mutagenesis screening conjunction with cross-species genomic transcriptomic validation, we identified strong consistent signal for neuronal, synaptic, glutamatergic signaling gene sets murine human SCLC. We show that SCLC cells have the ability to develop intimate contacts neuronal...
Abstract Integration of new neurons into adult hippocampal circuits is a process coordinated by local and long-range synaptic inputs. To achieve stable integration uniquely contribute to function, immature are endowed with critical period heightened plasticity, yet it remains unclear which mechanisms sustain this form plasticity during neuronal maturation. We found that, as enter their period, transient surge in fusion dynamics stabilizes elongated mitochondrial morphologies dendrites fuel...
Direct neuronal reprogramming is a promising approach to replace neurons lost due disease via the conversion of endogenous glia reacting brain injury into neurons. However, it essential demonstrate that newly generated originate from glial cells and/or show they are not pre-existing Here, we use controls for both requirements while comparing two viral vector systems (Mo-MLVs and AAVs) expression same neurogenic factor, phosphorylation-resistant form Neurogenin2. Our results Mo-MLVs targeting...
Abstract The transition between quiescence and activation in neural stem progenitor cells (NSPCs) is coupled to reversible changes energy metabolism with key implications for life-long NSPC self-renewal neurogenesis. How this metabolic plasticity ensured activity states unclear. We found that a state-dependent rewiring of the mitochondrial proteome by peptidase YME1L required preserve adult brain. YME1L-mediated regulates rate fatty acid oxidation (FAO) replenishing Krebs cycle intermediates...