Nicole Schröder

ORCID: 0009-0002-9030-9329
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About
Contact & Profiles
Research Areas
  • S100 Proteins and Annexins
  • Alzheimer's disease research and treatments
  • Bone Metabolism and Diseases
  • GDF15 and Related Biomarkers
  • Immune Response and Inflammation
  • Antimicrobial Peptides and Activities
  • Glutathione Transferases and Polymorphisms
  • Neuropeptides and Animal Physiology
  • Breast Lesions and Carcinomas
  • Cardiovascular Syncope and Autonomic Disorders
  • Advanced NMR Techniques and Applications
  • Education Methods and Technologies
  • Historical Studies on Reproduction, Gender, Health, and Societal Changes
  • Innovative Teaching Methodologies in Social Sciences
  • Sociology and Education Studies
  • Pharmaceutical Economics and Policy
  • Historical Gender and Feminism Studies
  • Second Language Learning and Teaching
  • Clinical practice guidelines implementation
  • Pneumonia and Respiratory Infections
  • Solid-state spectroscopy and crystallography
  • Genomics, phytochemicals, and oxidative stress
  • Pharmaceutical studies and practices
  • Crystallography and Radiation Phenomena
  • European history and politics

RWTH Aachen University
2018-2023

DIPF | Leibniz Institute for Research and Information in Education
2023

Universitätsklinikum Aachen
2022

University of Rostock
2020-2021

Otto-von-Guericke University Magdeburg
2014

Abstract Background An important hallmark of Alzheimer’s disease (AD) is the increase Aβ1-42 burden and its accumulation to senile plaques, leading reactive gliosis neurodegeneration. The modulation glia cell function represents an attractive therapeutic strategy, but currently limited by incomplete understanding relevance for AD. chemotactic G-protein coupled formyl peptide receptor (FPR), which known modulate uptake signal transduction, might be one candidate molecule regulating in Here,...

10.1186/s12974-020-01816-2 article EN cc-by Journal of Neuroinflammation 2020-04-24

Abstract The major histopathological hallmarks of Alzheimer’s disease (AD) include β-amyloid (Aβ) plaques, neurofibrillary tangles, and neuronal loss. Aβ 1–42 (Aβ 1-42 ) has been shown to induce neurotoxicity secretion proinflammatory mediators that potentiate neurotoxicity. Proinflammatory neurotoxic activities were be mediated by interactions with several cell surface receptors, including the chemotactic G protein-coupled N-formyl peptide receptor 2 (FPR2). present study investigated...

10.1007/s12035-021-02543-2 article EN cc-by Molecular Neurobiology 2021-09-01

Abstract Background Bacterial meningitis is still a cause of severe neurological disability. The brain protected from penetrating pathogens by the blood-brain barrier and innate immune system. invading are recognized pattern recognition receptors including G-protein-coupled formyl peptide (FPRs), which expressed cells central nervous FPRs show broad spectrum ligands, pro- anti-inflammatory ones. Here, we investigated effects annexin A1 mimetic Ac2-26 in mouse model pneumococcal meningitis....

10.1186/s12974-020-02006-w article EN cc-by Journal of Neuroinflammation 2020-10-29

The Nrf2 signaling pathway prevents cancer initiation, but genetic mutations that activate this are found in various types of cancer. molecular mechanisms underlying Janus-headed character still not understood. Here, we show sustained activation induces proliferation and dedifferentiation a Wnt-responsive perivenular hepatic progenitor cell population, transforming them into metastatic cells. neoplastic lesions display many histological features known from human hepatoblastoma. We describe...

10.1016/j.redox.2022.102453 article EN cc-by Redox Biology 2022-09-13

Einleitung: Das Liposarkom ist mit einer Inzidenz von etwa 2,5 Neuerkrankungen/1 Mio. Einwohner/Jahr eine seltene Erkrankung. Den einzigen kurativen Therapieansatz stellt die komplette Resektion dar. Aufgrund der oft retroperitonealen Lage werden Liposarkome meist erst im fortgeschrittenen Stadium diagnostiziert.

10.1055/s-0034-1386482 article DE Zeitschrift für Gastroenterologie 2014-08-11

Abstract Background: An important hallmark of Alzheimer's disease (AD) is the increase Aβ1-42 burden and its accumulation to senile plaques, leading reactive gliosis neurodegeneration. The modulation glia cell function represent an attractive therapeutic strategy, but currently limited by incomplete understanding relevance for AD. chemotactic G-protein coupled formyl peptide receptor (FPR), which known modulate uptake signal transduction, might be one candidate molecule regulating in Here,...

10.21203/rs.2.17967/v1 preprint EN cc-by Research Square (Research Square) 2019-12-03

Abstract Background: An important hallmark of Alzheimer's disease (AD) is the increase Aβ1-42 burden and its accumulation to senile plaques, leading reactive gliosis neurodegeneration. The modulation glia cell function represent an attractive therapeutic strategy, but currently limited by incomplete understanding relevance for AD. chemotactic G-protein coupled formyl peptide receptor (FPR), which known modulate uptake signal transduction, might be one candidate molecule regulating in Here,...

10.21203/rs.2.17967/v2 preprint EN cc-by Research Square (Research Square) 2020-03-30

Abstract BackgroundBacterial meningitis is, despite progress in research and the development of new treatment strategies, still a cause severe neurological disability. The brain is protected from penetrating pathogens by blood-brain barrier innate immune system. invading are recognized pattern recognition receptors including G-protein coupled formyl peptide (FPRs), which expressed cells central nervous FPRs show broad spectrum ligands pro- anti-inflammatory ones. Here, we investigated...

10.21203/rs.3.rs-28938/v1 preprint EN cc-by Research Square (Research Square) 2020-05-19
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