A5057937284- Neuroinflammation and Neurodegeneration Mechanisms
- Alzheimer's disease research and treatments
- Tryptophan and brain disorders
- Neurological Disease Mechanisms and Treatments
- Inflammation biomarkers and pathways
- Graphene and Nanomaterials Applications
- Phagocytosis and Immune Regulation
- Neonatal and fetal brain pathology
- Neurogenesis and neuroplasticity mechanisms
- Cholesterol and Lipid Metabolism
- Immune cells in cancer
- Inflammasome and immune disorders
UK Dementia Research Institute
2019-2024
University of Edinburgh
2019-2024
University of Manchester
2014-2016
University of Kentucky
2015
St. Clare Hospital in Lakewood
2015
Abstract Non-steroidal anti-inflammatory drugs (NSAIDs) inhibit cyclooxygenase-1 (COX-1) and COX-2 enzymes. The NLRP3 inflammasome is a multi-protein complex responsible for the processing of proinflammatory cytokine interleukin-1β implicated in many inflammatory diseases. Here we show that several clinically approved widely used NSAIDs fenamate class are effective selective inhibitors via inhibition volume-regulated anion channel macrophages, independently COX Flufenamic acid mefenamic...
Synapse loss correlates with cognitive decline in Alzheimer's disease (AD). Data from mouse models suggests microglia are important for synapse degeneration, but direct human evidence any glial involvement removal AD remains to be established. Here we observe astrocytes and brains contain greater amounts of synaptic protein compared non-disease controls, that proximity amyloid-β plaques the APOE4 risk gene exacerbate this effect. In culture, primary phagocytose patient-derived synapses more...
Microglia are considered the resident immune cells of central nervous system (CNS). In response to harmful stimuli, an inflammatory reaction ensues in which microglia activated a sequenced spectrum pro- and antiinflammatory phenotypes that akin well-characterized polarization states peripheral macrophages. A "classically" M1 phenotype is known eradicate toxicity. The transition "alternatively" M2 encompasses neuroprotection repair. recent years, inflammation has been accompanying pathology...
Summary Synapse loss correlates with cognitive decline in Alzheimer’s disease (AD). Data from mouse models suggests microglia are important for synapse degeneration, but direct human evidence any glial involvement removal AD remains to be established. Here we observe astrocytes and brains contain greater amounts of synaptic protein compared non-disease controls, that proximity amyloid-β plaques the APOE4 risk gene exacerbate this effect. In culture, primary phagocytose patient-derived...
Dementia is most often attributed to Alzheimer’s disease (~70%) or vascular dementia (~17%), yet 20-50% of cases share aspects both. Better understanding dementias within this spectrum can improve diagnosis, inform interpretation clinical data confounded by co-morbidity, and direct therapeutic approaches. We hypothesized that combined pathologies alter the time-course memory impairment expression primary pathology. compared cerebrovascular (chronic cerebral hypoperfusion) (transgene-driven...