Publications by authors named "A Wilken-Schmitz"

Background: COVID-19 is a serious viral infection, which is often associated with a lethal outcome. Therefore, understanding mechanisms, which affect the immune response during SARS-CoV2 infection, are important.

Methods: To address this, we determined the number of T cells in peripheral blood derived from intensive care COVID-19 patients.

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  • Progranulin (PGRN) is a neurotrophic and anti-inflammatory protein, and its loss due to human mutations is linked to frontotemporal dementia, with PGRN knockout (KO) mice used to model this condition.
  • Restoration of PGRN in neurons (but not microglia) was achieved in a specific mouse model, allowing researchers to investigate if it could reduce brain damage after traumatic brain injury (TBI).
  • Findings indicated that restoring PGRN in neurons was enough to mitigate excessive brain damage caused by TBI, suggesting that microglial PGRN was not necessary for neuroprotection and anti-inflammatory effects in this context.
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Epidemiological studies show a coincidence between Parkinson's disease (PD) and malignant melanoma. It has been suggested that this relationship is due, at least in part, to modulation of alpha-Synuclein (αSyn/Snca). αSyn oligomers accumulate in PD, which triggers typical PD symptoms, and in malignant melanoma, which increases the proliferation of tumor cells.

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Background: Pain in early life may impact on development and risk of chronic pain. We developed an optogenetic Cre/loxP mouse model of "early-life-pain" (ELP) using mice with transgenic expression of channelrhodopsin-2 (ChR2) under control of the Advillin (Avil) promoter, which drives expression of transgenes predominantly in isolectin B4 positive non-peptidergic nociceptors in postnatal mice. Avil-ChR2 (Cre +) and ChR2-flfl control mice were exposed to blue light in a chamber once daily from P1-P5 together with their Cre-negative mother.

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  • Rotenone was tested as a potential model for Parkinson's disease in mice using a daily oral regimen for 4 to 8 weeks.
  • The study assessed motor functions, neuron health, and inflammation but found no significant motor deficits or signs of neuronal degeneration in the rotenone-treated mice.
  • Analysis revealed that rotenone had insufficient bioavailability in the bloodstream, indicating the treatment caused gastrointestinal issues without producing typical Parkinson's disease symptoms.
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