A5025861227- Neuroinflammation and Neurodegeneration Mechanisms
- Alzheimer's disease research and treatments
- Neurogenesis and neuroplasticity mechanisms
- RNA regulation and disease
- Immune cells in cancer
- RNA Research and Splicing
- Genetic and Clinical Aspects of Sex Determination and Chromosomal Abnormalities
- Systemic Lupus Erythematosus Research
- Adenosine and Purinergic Signaling
- Axon Guidance and Neuronal Signaling
- Nerve injury and regeneration
- Neuroscience and Neuropharmacology Research
- MicroRNA in disease regulation
- Antimicrobial Peptides and Activities
- Tryptophan and brain disorders
- Monoclonal and Polyclonal Antibodies Research
- Galectins and Cancer Biology
- Endoplasmic Reticulum Stress and Disease
- Sperm and Testicular Function
- RNA and protein synthesis mechanisms
- Genetics and Neurodevelopmental Disorders
- Liver Disease Diagnosis and Treatment
- Pancreatic function and diabetes
- Metabolism, Diabetes, and Cancer
University of Bonn
2021-2025
German Center for Neurodegenerative Diseases
2018-2022
Center of Advanced European Studies and Research
2016
Reactive astrogliosis is a hallmark of Alzheimer's disease (AD), but its role for initiation and progression has remained incompletely understood. We here show that the transcription factor Stat3 (signal transducer activator 3), canonical inducer astrogliosis, activated in an AD mouse model human Therefore, using conditional knockout approach, we deleted specifically astrocytes APP/PS1 found Stat3-deficient mice decreased β-amyloid levels plaque burden. Plaque-close microglia displayed more...
Astrocytes support normal brain function, but may also contribute to neurodegeneration when they become reactive under pathological conditions such as stroke. However, the molecular underpinnings of this context-dependent interplay between beneficial and detrimental properties in astrogliosis have remained incompletely understood. Therefore, using RiboTag technique, we immunopurified translating mRNAs specifically from astrocytes 72 hr after transient middle cerebral artery occlusion mice...
Astrocytic hyperactivity is an important contributor to neuronal-glial network dysfunction in Alzheimer’s disease (AD). We have previously shown that astrocyte mediated by signaling through the P2Y1 purinoreceptor (P2Y1R) pathway. Using APPPS1 mouse model of AD, we here find chronic intracerebroventricular infusion P2Y1R inhibitors normalizes astroglial and neuronal dysfunction, as measured vivo two-photon microscopy, augments structural synaptic integrity, preserves hippocampal long-term...
Alzheimer's disease (AD) is characterized by two neuropathological hallmarks: senile plaques, which are composed of amyloid-β (Aβ) peptides, and neurofibrillary tangles, hyperphosphorylated tau protein. Aβ peptides derived from sequential proteolytic cleavage the amyloid precursor protein (APP). In this study, we identified a so far unknown mode regulation APP synthesis involving MID1 complex: binds to regulates translation mRNA. The underlying action involves mTOR pathway. Thus, inhibition...
In central nervous system (CNS) diseases characterized by late-onset neurodegeneration, the interplay between innate and adaptive immune responses remains poorly understood. This knowledge gap is exacerbated prolonged protracted disease course as it complicates delineation of brain-resident infiltrating cells. Here, we conducted comprehensive profiling cells in a murine model spastic paraplegia 15 (SPG15), complicated form hereditary paraplegia. Using fate-mapping bone marrow–derived cells,...
The unfolded protein response (UPR) is associated with hepatic metabolic function, yet it not well understood how endoplasmic reticulum (ER) disturbance might influence homeostasis. Here, we describe the physiological function of Cysteine-rich EGF-like domains 2 (Creld2), previously characterized as a downstream target ER-stress signal transducer Atf6. To this end, generated Creld2-deficient mice and induced UPR by injection tunicamycin. Creld2 augments folding creates an interlink between...
Abstract Genetic variation is a primary determinant of phenotypic diversity. In laboratory mice, genetic can be serious experimental confounder, and thus minimized through inbreeding. However, generalizations results obtained with inbred strains must made caution, especially when working complex phenotypes disease models. Here we compared behavioral characteristics C57Bl/6—the strain most widely used in biomedical research—with those 129S4. contrast to 129S4, C57Bl/6 demonstrated high...
Ischaemic stroke remains a leading cause of death and disability worldwide. Surviving neurons in the peri-infarct area are able to establish novel axonal projections juxtalesional regions, but this regeneration is curtailed by growth-inhibitory environment induced cells such as reactive astrocytes glial scar. Here, we found that astroglial synaptogenic cue thrombospondin-1 upregulated area, hence tested effects anticonvulsant pregabalin, blocker neuronal receptor Alpha2delta1/2, mouse model...
A bstract Genetic variation is a primary determinant of phenotypic diversity within populations. In laboratory mice, genetic has often been regarded as serious experimental confounder, and thus minimized through inbreeding. However, generalizations results obtained with inbred strains need to be made caution. Effects background on traits controlled, especially when working complex phenotypes disease models. Here we compared behavioral parameters C57Bl/6 – the mouse strain most widely used...
<h3>Background</h3> Systemic lupus erythematosus (SLE) is an autoimmune disease characterised by a wide range of antibodies reacting with nuclear antigens. Abnormalities in the apoptotic cell death process and clearance may play important role generating these antibodies. Especially to histones serum are frequently associated SLE. <h3>Objectives</h3> The aims this study were evaluate presence cytoplasm fresh peripheral blood mononuclear cells (PBMCs) activated lymphoblasts. lymphoblasts...