A5046607501- Alzheimer's disease research and treatments
- Neuroinflammation and Neurodegeneration Mechanisms
- Cerebrovascular and genetic disorders
- Spinal Dysraphism and Malformations
- Advanced Proteomics Techniques and Applications
- Plant Gene Expression Analysis
- Autoimmune and Inflammatory Disorders Research
- Advanced Glycation End Products research
- Plant-Microbe Interactions and Immunity
- Cellular transport and secretion
- Plant Stress Responses and Tolerance
- Lymphatic System and Diseases
- Fetal and Pediatric Neurological Disorders
- Barrier Structure and Function Studies
- Prenatal Screening and Diagnostics
- Neurological diseases and metabolism
- Lysosomal Storage Disorders Research
- Neuroscience and Neuropharmacology Research
German Center for Neurodegenerative Diseases
2021-2025
Technical University of Munich
2024-2025
Ludwig-Maximilians-Universität München
2024
Klinikum rechts der Isar
2024
Friedrich-Alexander-Universität Erlangen-Nürnberg
2019
The β-secretase β-site APP cleaving enzyme (BACE1) is a central drug target for Alzheimer's disease. Clinically tested, BACE1-directed inhibitors also block the homologous protease BACE2. Yet little known about physiological BACE2 substrates and functions in vivo. Here, we identify as shedding lymphangiogenic vascular endothelial growth factor receptor 3 (VEGFR3). Inactivation of BACE2, but not BACE1, inhibited VEGFR3 from primary human lymphatic cells (LECs) reduced release shed, soluble...
Summary Arabidopsis plants overexpressing glycolate oxidase in chloroplasts (GO5) and loss‐of‐function mutants of the major peroxisomal catalase isoform, cat2‐2 , produce increased hydrogen peroxide (H 2 O ) amounts from respective organelles when subjected to photorespiratory conditions like light intensity. Here, we have investigated if how signaling processes triggered by H production response shifts environmental concomitant induction indole phytoalexin biosynthesis GO5 affect...
The membrane protein seizure 6-like (SEZ6L) is a neuronal substrate of the Alzheimer's disease protease BACE1, and little known about its physiological function in nervous system. Here, we show that SEZ6L constitutive knockout mice display motor phenotypes adulthood, including changes gait decreased coordination. Additionally, displayed increased anxiety-like behaviour, although spatial learning memory Morris water maze were normal. Analysis gross anatomy proteome adult cerebellum did not...
Loss-of-function mutations in the homotrimeric serine protease HTRA1 cause cerebral vasculopathy. Here, we establish independent approaches to achieve functional correction of trimer assembly defects. Focusing on prototypical R274Q mutation, identify an variant that promotes formation thus restoring enzymatic activity vitro. Genetic experiments Htra1
Niemann-Pick type C (NPC) disease is an inherited lysosomal storage disorder mainly driven by mutations in the NPC1 gene, causing lipid accumulation within late endosomes/lysosomes and resulting progressive neurodegeneration. Although microglial activation precedes neuronal loss, it remains elusive whether loss of membrane protein microglia actively contributes to NPC pathology. In a mouse model with depletion myeloid cells, we report severe alterations lipidomic profiles, including...