A5028848708- Alzheimer's disease research and treatments
- Tryptophan and brain disorders
- Neuroinflammation and Neurodegeneration Mechanisms
- Nuclear Receptors and Signaling
- Coagulation, Bradykinin, Polyphosphates, and Angioedema
- S100 Proteins and Annexins
- Neurogenesis and neuroplasticity mechanisms
- Advanced Glycation End Products research
- Memory and Neural Mechanisms
- Cancer, Stress, Anesthesia, and Immune Response
- PI3K/AKT/mTOR signaling in cancer
- Neuroscience and Neuropharmacology Research
- Adenosine and Purinergic Signaling
- Prion Diseases and Protein Misfolding
- Cholinesterase and Neurodegenerative Diseases
- Stress Responses and Cortisol
- Neuroendocrine regulation and behavior
- Phosphodiesterase function and regulation
- Receptor Mechanisms and Signaling
- Neuropeptides and Animal Physiology
- Axon Guidance and Neuronal Signaling
- Ion channel regulation and function
- Birth, Development, and Health
- Apelin-related biomedical research
- Renal and related cancers
University of Duisburg-Essen
2015-2023
Essen University Hospital
2011-2020
Institute of Neurobiology
2009-2019
University Hospital Münster
2006-2009
University of Münster
2007
St Thomas' Hospital
1964
Alterations in the expression of Reelin (RELN) have been implicated pathology Alzheimer's disease (AD). However, whether these changes are cause or consequence AD remains to be resolved. To better understand role RELN pathway t
Physical activity protects brain function in healthy individuals and those with Alzheimer's disease (AD). Evidence for beneficial effects of parental exercise on the health status their progeny is sparse limited to nondiseased individuals. Here, we questioned whether maternal running interferes offspring's AD-like pathology sought decipher underlying mechanisms TgCRND8 mice. Maternal stimulation was provided by voluntary wheel vs. standard housing during pregnancy. Following 5 mo transgenic...
Abstract Despite amyloid plaques, consisting of insoluble, aggregated amyloid-β peptides, being a defining feature Alzheimer’s disease, their significance has been challenged due to controversial findings regarding the correlation cognitive impairment in disease with plaque load. The cascade hypothesis defines soluble oligomers, multiple monomers, as precursors insoluble plaques. Dissecting biological effects single for example dimers, an abundant oligomer associated clinical progression...
Oxidative stress is a key feature during progression of chronic neurodegenerative conditions such as Alzheimer's disease. In aging humans and animals, voluntary exercise lowers oxidative reactions. Additionally, recent work in our lab demonstrated that cognitive physical stimulation (termed environmental enrichment) counteracts amyloid beta pathology, neurovascular dysfunction behavioral symptoms mice with Alzheimer-like Based on these facts, we hypothesized activity can also protect against...
We and others have recently demonstrated that cognitive physical stimulation in form of environmental enrichment reduces cerebral β‐amyloid (Aβ) deposition transgenic mouse models Alzheimer’s disease. This effect was independent from amyloid precursor protein (APP) expression or processing rather a consequence enhanced clearance Aβ. However, the detailed mechanisms remain unclear. In present study, we show TgCRND8 mice (carrying human APP Swedish+Indiana ) affect neurovascular unit by...
Memory loss and increased anxiety are clinical hallmarks of Alzheimer's disease (AD). Kallikrein-8 is a protease implicated in memory acquisition anxiety, its mRNA known to be up-regulated AD-affected human hippocampus. Therefore, an involvement pathogenesis conceivable but remains proved.We determined the cerebral expression protein during course AD patients transgenic mice tested impact inhibition on AD-related pathology primary glial cells.Kallikrein-8 were both species at incipient...
Clinical data indicate that therapy with small-molecule immunosuppressive drugs is frequently accompanied by an incidence rate of neuropsychiatric symptoms. In the current approach, we investigated in rats whether repeated administration rapamycin, reflecting clinical conditions patients undergoing this mammalian target rapamycin inhibitor, precipitates changes neurobehavioral functioning.Male adult Dark Agouti were daily treated i.p. injections (1, 3 mg/kg) or vehicle for 8 days. On days 6...
Abstract Women seem to have a higher vulnerability Alzheimer's disease (AD), but the underlying mechanisms of this sex dichotomy are not well understood. Here, we first determined influence on various aspects pathology in transgenic CRND8 mice. We demonstrate that beta‐amyloid (Aβ) plaque burden starts be more severe around P180 (moderate stage) female transgenics when compared males and aging aggravates sex‐specific difference. Furthermore, show suffer from levels neurovascular dysfunction...
Objective There is still an urgent need for supportive minimally invasive and cost-effective biomarkers early diagnosis of Alzheimer’s disease (AD). Previous work in our lab has identified Kallikrein-8 (KLK8) as a potential candidate since it shows excessive increase human brain preclinical stages. The aim this study was to evaluate the diagnostic performance cerebrospinal fluid (CSF) blood KLK8 AD mild cognitive impairment (MCI) due AD. Methods In multi-centre trans-sectional study,...
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)),...
Sympathetic nerve stimulation causes a constriction of submucosal arterioles that is mediated by ATP acting at P2 receptors. In the present study, we examined receptor subtype mediating this response. A computer-assisted video monitoring system measured drug-induced changes in arteriolar diameter (resting approximately 40-80 microns) pieces submucosa vitro. The rank-order potency for vasoconstriction caused several analogs was alpha,beta-methylene (alpha,beta-MeATP) > beta,gamma-methylene =...
Previous work in our lab has identified the protease kallikrein-8 (KLK8) as a potential upstream mover pathogenesis of Alzheimer's disease (AD). We showed pathologically elevated levels KLK8 cerebrospinal fluid and blood patients with mild cognitive impairment or dementia due to AD, brains transgenic CRND8 (TgCRND8) mice incipient stages disease. Furthermore, short-term antibody-mediated inhibition moderate stage alleviated AD pathology female mice. However, it remains be shown whether...
Abstract Objectives The heterogeneity of Amyloid‐beta (Aβ) plaque load in patients with Alzheimer's disease (AD) has puzzled neuropathology. Since brain Aβ does not correlate cognitive decline, neurotoxic soluble oligomers have been championed as disease‐causing agents early AD. So far, investigating molecular interactions between oligomeric and insoluble vivo difficult because the abundance oligomer species kinetic equilibrium which they coexist. Here, we investigated whether relates to...