A5000549309- Neuroinflammation and Neurodegeneration Mechanisms
- Long-Term Effects of COVID-19
- Neuropeptides and Animal Physiology
- Inflammasome and immune disorders
- Amyotrophic Lateral Sclerosis Research
- Neuroscience and Neuropharmacology Research
- Complement system in diseases
- Neurogenesis and neuroplasticity mechanisms
- Tryptophan and brain disorders
- Stress Responses and Cortisol
- Receptor Mechanisms and Signaling
- COVID-19 and Mental Health
- Neurogenetic and Muscular Disorders Research
The University of Queensland
2019-2024
Coronavirus disease-2019 (COVID-19) is primarily a respiratory disease, however, an increasing number of reports indicate that SARS-CoV-2 infection can also cause severe neurological manifestations, including precipitating cases probable Parkinson's disease. As microglial NLRP3 inflammasome activation major driver neurodegeneration, here we interrogated whether promote activation. Using transgenic mice expressing human angiotensin-converting enzyme 2 (hACE2) as COVID-19 pre-clinical model,...
Accumulating evidence underscores the pivotal role of heightened inflammation in pathophysiology stress-related diseases, yet underlying mechanisms remain elusive. The complement system, a key effector innate immune produces C5-cleaved activation product C5a upon activation, initiating inflammatory responses through canonical receptor 1 (C5aR1). While C5aR1 is expressed stress-responsive brain regions, its stress responsiveness remains unknown. To investigate C5a-C5aR1 signaling responses,...
ABSTRACT Coronavirus disease-2019 (COVID-19) is primarily a respiratory disease, however, an increasing number of reports indicate that SARS-CoV-2 infection can also cause severe neurological manifestations, including precipitating cases probable Parkinson’s disease. As microglial NLRP3 inflammasome activation major driver neurodegeneration, here we interrogated whether promote utilising model human monocyte-derived microglia. We identified isolates bind and enter microglia, triggering in...