A5057686813- Cellular transport and secretion
- Tryptophan and brain disorders
- Neuroendocrine regulation and behavior
- Retinal Development and Disorders
- Botulinum Toxin and Related Neurological Disorders
- Neuroinflammation and Neurodegeneration Mechanisms
- Acute Ischemic Stroke Management
- Lipid Membrane Structure and Behavior
- Endoplasmic Reticulum Stress and Disease
- Pancreatic function and diabetes
- Stress Responses and Cortisol
- Microtubule and mitosis dynamics
- Alzheimer's disease research and treatments
- Neuroscience and Neuropharmacology Research
- Stroke Rehabilitation and Recovery
Cologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases
2020-2023
University of Cologne
2020-2023
Essen University Hospital
2020
Cleavage of amyloid precursor protein (APP) by BACE-1 (β-site APP cleaving enzyme 1) is the rate-limiting step in amyloid-β (Aβ) production and a neuropathological hallmark Alzheimer's disease (AD). Despite decades research, mechanisms amyloidogenic processing remain highly controversial. Here, we show that neurons, Aβ are controlled complex-2 (AP-2), an endocytic adaptor known to be required for endocytosis. Now, find AP-2 prevents amyloidogenesis additionally functioning downstream BACE1...
Abstract Disrupted neuronal plasticity due to subtle inflammation is considered play a fundamental role in the pathogenesis of major depressive disorder. Interferon-α (IFN-α) potentiates immune responses against viral pathogens that induce toll-like receptor-3 (TLR3) activation but evokes severe disorder humans by mechanisms remain insufficiently described. By using previously established mouse model depression induced combined delivery IFN-α and polyinosinic:polycytidylic acid (poly(I:C)),...
Centrosomes are organelles that nucleate microtubules via the activity of gamma–tubulin ring complexes (γ-TuRC). In developing brain, centrosome integrity is central to progression neural progenitor cell cycle, and its loss leads microcephaly. We show NPCs maintain endocytic adaptor protein complex-2 (AP-2). lacking AP-2 exhibit defects in formation mitotic progression, accompanied by DNA damage accumulation p53. This function regulating proliferative capacity independent role...