Thomas Blank

ORCID: 0000-0002-3969-405X
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About
Contact & Profiles
Research Areas
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Neuroscience and Neuropharmacology Research
  • Tryptophan and brain disorders
  • Immune cells in cancer
  • Stress Responses and Cortisol
  • Alzheimer's disease research and treatments
  • Ion channel regulation and function
  • Gut microbiota and health
  • Receptor Mechanisms and Signaling
  • Immune Response and Inflammation
  • Memory and Neural Mechanisms
  • Escherichia coli research studies
  • Bacillus and Francisella bacterial research
  • Hormonal Regulation and Hypertension
  • Bacteriophages and microbial interactions
  • Neurogenesis and neuroplasticity mechanisms
  • Long-Term Effects of COVID-19
  • Bacterial Genetics and Biotechnology
  • Neuroendocrine regulation and behavior
  • interferon and immune responses
  • Probiotics and Fermented Foods
  • Cholinesterase and Neurodegenerative Diseases
  • Viral gastroenteritis research and epidemiology
  • NF-κB Signaling Pathways
  • Nicotinic Acetylcholine Receptors Study

University of Freiburg
2015-2024

University Medical Center Freiburg
2015-2019

Institute of Neuroimmunology of the Slovak Academy of Sciences
2019

University of Hawaiʻi at Mānoa
2006-2015

United States Army Medical Research Institute of Infectious Diseases
2006-2008

Icahn School of Medicine at Mount Sinai
2008

Hershey (United States)
2008

Pennsylvania State University
1994-2008

The Ohio State University
2008

Massachusetts General Hospital
2008

In the present experiments, we characterized action of human/rat corticotropin-releasing factor (h/rCRF) and acute stress (1 hr immobilization) on hippocampus-dependent learning synaptic plasticity in mouse hippocampus. We first showed that h/rCRF application facilitated (primed) long-term potentiation population spikes (PS-LTP) hippocampus enhanced context-dependent fear conditioning. Both priming PS-LTP improvement conditioning were prevented by CRF receptor antagonist...

10.1523/jneurosci.22-09-03788.2002 article EN Journal of Neuroscience 2002-05-01

Corticotropin-releasing factor (CRF) exerts a key neuroregulatory control on stress responses in various regions of the mammalian brain, including hippocampus. Using hippocampal slices, extracts, and whole animals, we investigated effects human/rat CRF (h/rCRF) neuronal excitability hippocampus-dependent learning two mouse inbred strains, BALB/c C57BL/6N. Intracellular recordings from slices revealed that application h/rCRF increased activity both strains. Inhibition protein kinase C (PKC)...

10.1523/jneurosci.23-02-00700.2003 article EN Journal of Neuroscience 2003-01-15

Abstract TGFβ1 has been implicated in regulating functional aspects of several distinct immune cell populations including central nervous system (CNS) resident microglia. Activation and priming microglia have demonstrated to contribute the progression neurodegenerative diseases and, thus, underlie stringent control by endogenous regulatory factors TGFβ1. Here, we demonstrate that deletion Tgfbr2 adult postnatal does neither result impairment microglia-specific gene expression signatures, nor...

10.1038/s41467-018-06224-y article EN cc-by Nature Communications 2018-09-25

Abstract It was recently revealed that gut microbiota promote amyloid-beta (Aβ) burden in mouse models of Alzheimer’s disease (AD). However, the underlying mechanisms when using either germ-free (GF) housing conditions or treatments with antibiotics (ABX) remained unknown. In this study, we show GF and ABX-treated 5x familial AD (5xFAD) mice developed attenuated hippocampal Aβ pathology associated neuronal loss, thereby delayed disease-related memory deficits. While production unaffected...

10.1186/s40478-020-00988-5 article EN cc-by Acta Neuropathologica Communications 2020-07-29

Alzheimer's disease (AD) is characterized by severe neuronal loss as well the accumulation of amyloid-β (Aβ), which ultimately leads to plaque formation. Although there now a general agreement that aggregation Aβ can be initiated prion-like seeding, impact and functional consequences induced deposits (Aβ seeding) on neurons still remain open questions. Here, we find representing early stages formation, dramatic decrease in proliferation neurogenesis two APP transgenic mouse models. We...

10.15252/embj.201797021 article EN cc-by-nc-nd The EMBO Journal 2017-12-11

The signal transduction pathway underlying the cAMP-dependent modulation of rat striatal N -methyl- d -aspartate (NMDA) responses was investigated by using two-electrode voltage-clamp technique. In oocytes injected with poly(A) + mRNA, activation protein kinase (PKA) forskolin potentiated NMDA responses. Inhibition phosphatase 1 (PP1) and/or 2A (PP2A) specific inhibitor calyculin A occluded PKA-mediated potentiation responses, suggesting that PKA effect mediated inhibition a phosphatase....

10.1073/pnas.94.26.14859 article EN Proceedings of the National Academy of Sciences 1997-12-23

ABSTRACT Enteropathogenic Escherichia coli (EPEC) infections are a leading cause of infantile diarrhea in developing nations. Typical EPEC isolates differentiated from other types pathogenic E. by two distinctive phenotypes, attaching effacement and localized adherence. The genes specifying these phenotypes found on the locus enterocyte (LEE) adherence factor (EAF) plasmid. To describe how typical has evolved, we characterized diverse collection strains multilocus sequence typing (MLST)...

10.1128/jb.01472-06 article EN Journal of Bacteriology 2006-11-14

The IκB kinase complex induces nuclear factor kappa B activation and has recently been recognized as a key player of autoimmunity in the central nervous system. Notably, kinase/nuclear signalling regulates peripheral myelin formation by Schwann cells, however, its role system during health disease is largely unknown. Surprisingly, we found that brain-specific 2 expression dispensable for proper assembly repair system, but instead plays fundamental loss cuprizone model. During toxic...

10.1093/brain/awq359 article EN Brain 2011-02-11

Homo and heterozygote cx3cr1 mutant mice, which harbor a green fluorescent protein (EGFP) in their loci, represent widely used animal model to study microglia peripheral myeloid cells. Here we report that the dentate gyrus (DG) of −/− mice displayed elevated microglial sirtuin 1 (SIRT1) expression levels nuclear factor kappa-light-chain-enhancer activated B cells (NF-kB) p65 activation, despite unaltered morphology when compared +/− or +/+ controls. This phenotype was restricted DG...

10.1186/s40478-016-0374-8 article EN cc-by Acta Neuropathologica Communications 2016-09-17
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