A5041752446- Neuroinflammation and Neurodegeneration Mechanisms
- Alzheimer's disease research and treatments
- Gut microbiota and health
- Advanced Drug Delivery Systems
- COVID-19 Impact on Reproduction
- Complement system in diseases
- Neuropeptides and Animal Physiology
- Neuroscience and Neuropharmacology Research
- Analytical Chemistry and Sensors
- 14-3-3 protein interactions
- Nutrition, Genetics, and Disease
- Piperaceae Chemical and Biological Studies
- Anodic Oxide Films and Nanostructures
- Tryptophan and brain disorders
- Microfluidic and Bio-sensing Technologies
- Electrical and Bioimpedance Tomography
- Barrier Structure and Function Studies
University of California, Irvine
2021-2024
University of Madras
2007-2008
The complement system is part of the innate immune that clears pathogens and cellular debris. In healthy brain, influences neurodevelopment neurogenesis, synaptic pruning, clearance neuronal blebs, recruitment phagocytes, protects from pathogens. However, excessive downstream activation leads to generation C5a, C5a engagement with its receptor C5aR1, instigates a feed-forward loop inflammation, injury, death, making C5aR1 potential therapeutic target for neuroinflammatory disorders. ablation...
Abstract Multiple studies have recognized the involvement of complement cascade during Alzheimer’s disease pathogenesis. However, specific role C5a-C5aR1 signaling in progression this neurodegenerative is still not clear. Furthermore, its potential as a therapeutic target to treat AD remains be elucidated. Canonically, generation anaphylatoxin C5a result activation and interaction with receptor C5aR1 triggers potent inflammatory response. Previously, genetic ablation mouse model exerted...
Synaptic loss is a hallmark of Alzheimer's disease (AD) that correlates with cognitive decline in AD patients. Complement-mediated synaptic pruning has been associated this excessive synapses AD. Here, we investigated the effect C5aR1 inhibition on microglial and astroglial two mouse models
The contribution of the gut microbiome to neuroinflammation, cognition, and Alzheimer's disease progression has been highlighted over past few years. Additionally, inhibition various components complement system repeatedly demonstrated reduce neuroinflammation improve cognitive performance in AD mouse models. Whether deletion these is associated with distinct composition, which could impact models not yet examined. Here, we provide a comprehensive analysis conditional constitutive knockouts,...
Synaptic loss is a hallmark of Alzheimer's disease (AD) that correlates with cognitive decline in AD patients. Complement-mediated synaptic pruning has been associated this excessive synapses AD. Here, we investigated the effect C5aR1 inhibition on microglial and astroglial two mouse models
Abstract Background The complement system is part of the innate immune that clears pathogens and cellular debris. In healthy brain, influences neurodevelopment neurogenesis, synaptic pruning, clearance neuronal blebs, recruitment phagocytes, protects from pathogens. However, excessive downstream activation leads to generation C5a, C5a engagement with its receptor C5aR1, instigates a feed-forward loop inflammation, injury, death, making C5aR1 potential therapeutic target for neuroinflammatory...
Electrical impedance scanning (EIS) is a new technique in which moderate variations capacitance values are reflected by the cells of various type normal membrane. The malignant membrane vascular endothelial cell association with VEGF (vascular growth factor), contrast, EIS demonstrates significant relaxation phenomena concomitant α-dispersion low audio frequency range. author has endeavoured to establish above stated phenomena. In this experimental setup, lipo-protein constituent was...
Abstract Multiple studies have recognized the involvement of complement cascade during Alzheimer’s disease pathogenesis; however, specific role C5a-C5aR1 signaling in progression this neurodegenerative is still not clear. Furthermore, its potential as a therapeutic target to treat AD remains be elucidated. Canonically, generation anaphylatoxin C5a result activation and interaction with receptor C5aR1 triggers potent inflammatory response. Previously, genetic ablation mouse model exerted...
Abstract Background The complement (C’) system contributes to enhanced inflammation and cognitive decline in Alzheimer’s disease (AD). Previous studies demonstrated that genetic ablation of downstream receptor C5aR1 provides protection from AD animal models. C’ activation associated cell‐signaling may influence the composition gut microbiome, modulating systemic inflammation, ultimately inducing behavioral changes. objective this study was determine if deletion (C5aR1KO) alters fecal...
The complement system, a powerful effector mechanism of the immune can be activated by fAβ, leading to generation C5a. Upon binding its microglial receptor (C5aR1), C5a-C5aR1 signaling cascade contributes neuroinflammation. Previous results have shown beneficial effect blocking in Alzheimer's disease (AD), either genetic ablation C5aR1 or using pharmacological approach. Here, we further examined antagonist (PMX205) on amyloid pathology and glial activation progression mouse model AD.Tg2576...
Alzheimer's disease (AD) is the most prevalent form of dementia elderly in US. No disease-modifying drugs have been approved, indicating a need for novel targets and relevant biomarkers to follow treatment efficacy. Neurofilament-light (NfL) an intermediate filament protein neurons that increases plasma after injury neurodegeneration, suggesting it may be biomarker neurodegeneration before other symptoms are evident. Here, we measured blood NfL levels Arctic AD mouse compared neuroprotective...