Publications by authors named "A Ergul"
Article Synopsis
- mPGES-1 is highlighted as a key target for developing treatments for inflammation and pain, with the study introducing new benzimidazole compounds that effectively inhibit this enzyme.
- One of the compounds, AGU654, showed exceptional selectivity for mPGES-1 over other related enzymes, with a low inhibition concentration (IC = 2.9 nM) and promising bioavailability.
- AGU654 was able to reduce PGE production from activated immune cells without affecting other prostaglandins, and it also demonstrated success in alleviating fever and pain in guinea pig models, indicating its potential for managing inflammatory diseases.
Diabetes is a major risk factor for all types of dementia. The underlying reasons are not fully understood, and preventive therapeutic strategies are lacking. Previously we have shown that diabetic but not control rats developed a progressive cognitive decline in a microemboli (ME) model of vascular contributions to cognitive impairment & dementia (VCID).
View Article and Find Full Text PDFEndothelin-1 (ET-1), the most potent vasoconstrictor identified to date, contributes to cerebrovascular dysfunction. ET-1 levels in postmortem brain specimens from individuals diagnosed with Alzheimer's disease (AD) and related dementias (ADRD) were shown to be related to cerebral hypoxia and disease severity. ET-1-mediated vascular dysfunction and ensuing cognitive deficits have also been reported in experimental models of AD and ADRD.
View Article and Find Full Text PDFArticle Synopsis
- Diabetes can lead to endothelial dysfunction and increase the risk of Alzheimer's disease by dysregulating the endothelin (ET) system, particularly ET-1's effect on brain microvascular pericytes (BMVPCs).
- In experiments mimicking diabetic conditions, ET-1 was found to induce cellular senescence in BMVPCs, evidenced by increased senescence markers and altered cellular phenotype, showing a potential link between ET-1 and inflammatory responses.
- The study suggests that blocking ETA receptors can mitigate the effects of ET-1 on BMVPCs, indicating that further in vivo research is necessary to understand the implications for vascular cognitive impairment and dementia (VCID).