A5037020727- Neuroinflammation and Neurodegeneration Mechanisms
- S100 Proteins and Annexins
- Long-Term Effects of COVID-19
- Neurological Disease Mechanisms and Treatments
- Neurological Disorders and Treatments
- Acute Ischemic Stroke Management
- Inflammasome and immune disorders
- Tryptophan and brain disorders
- Alzheimer's disease research and treatments
- Heme Oxygenase-1 and Carbon Monoxide
- COVID-19 Clinical Research Studies
- Redox biology and oxidative stress
- Signaling Pathways in Disease
- Extracellular vesicles in disease
- Adipose Tissue and Metabolism
- Renin-Angiotensin System Studies
- Traumatic Brain Injury and Neurovascular Disturbances
- Intracerebral and Subarachnoid Hemorrhage Research
- Advanced Glycation End Products research
- Nerve injury and regeneration
- Vagus Nerve Stimulation Research
- Phagocytosis and Immune Regulation
- Mitochondrial Function and Pathology
- HIV-related health complications and treatments
- Genomics, phytochemicals, and oxidative stress
Tulane University
2022-2025
University of Tennessee Health Science Center
2018-2024
Indiana University Bloomington
2024
Massachusetts General Hospital
2024
Sree Chitra Thirunal Institute for Medical Sciences and Technology
2015-2020
University of Memphis
2020
Activation of the NOD-like receptor protein (NLRP3)-inflammasome has been postulated to mediate inflammatory responses brain damage during ischemic/reperfusion (I/R) injury. We therefore hypothesized that MCC950, a selective NLRP3-inflammasome inhibitor provides protection in mouse model transient middle cerebral artery occlusion (tMCAO). Focal ischemia was induced by 60 min tMCAO followed intraperitoneal administration MCC950 (50 mg/kg) or saline at 1 h and 3 post-occlusion. After 24 I/R,...
Nucleotide oligomerization domain (NOD)-like receptor protein-3 (NLRP3) inflammasome may intimately contribute to sustaining damage after traumatic brain injury (TBI). This study aims examine whether specific modulation of NLPR3 by MCC950, a novel selective NLRP3 inhibitor, confers protection experimental TBI. Unilateral cortical impact was induced in young adult C57BL/6 mice. MCC950 (50 mg/kg, intraperitoneally) or saline administration at 1 and 3 h post-TBI. Animals were tested for...
Alzheimer's disease (AD) is the most common form of age-associated dementia characterized by amyloid-β plaques and neurofibrillary tangles. Recent studies have demonstrated that thioredoxin-interacting protein (TXNIP), an endogenous regulator redox/glucose induced stress inflammation, now known to be upregulated in stroke, traumatic brain injury, diabetes AD. We hypothesized TXNIP overexpression sustains neurodegeneration through activation nucleotide binding oligomerization domain-like...
Although the precise mechanisms contributing to secondary brain injury following traumatic are complex and obscure, a number of studies have demonstrated that inflammatory responses an obvious early feature in pathogenesis injury. Inflammasomes multiprotein complexes prompt stimulation caspase-1 subsequently induce maturation secretion proinflammatory cytokines, such as interleukin-1β interleukin-18. These cytokines play pivotal role facilitating innate immune inflammation. Among various...
Vascular cognitive impairment and dementia (VCID) is the second most common form of after Alzheimer's disease (AD). Currently, mechanistic insights into evolution progression VCID remain elusive. White matter change represents an invariant feature. Compelling clinical neuroimaging pathological evidence suggest a link between white changes neurodegeneration. Our prior study detected hypoperfused lesions in mice with partial deficiency endothelial nitric oxide (eNOS) at very young age,...
Aging is a known co-morbidity of ischemic stroke with its risk and severity increasing every year past 55+. While many the current therapies have shown success in reducing mortality, post-stroke morbidity has not seen same substantial reduction. Recently, involvement cellular senescence SASP brain injury neurological degeneration been recognized. Ischemic causes oxidative stress mitochondrial damage that induces through activation p21 p16 pathways, ultimately leading to synthesis release...
Increasing evidence suggests that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection impacts neurological function both acutely and chronically, even in the absence of pronounced distress. Developing clinically relevant laboratory mouse models neuropathogenesis SARS-CoV-2 is an important step toward elucidating underlying mechanisms SARS-CoV-2-induced dysfunction. Although various transgenic viral delivery methods have been used to study potential mice, use commonly...
Immune system hypersensitivity is believed to contribute mental frailty in the elderly. Solid evidence indicates NOD-like receptor pyrin domain containing-3 (NLRP3)-inflammasome activation intimately connects aging-associated chronic inflammation (inflammaging) senile cognitive decline. Thioredoxin interacting protein (TXNIP), an inducible involved oxidative stress, essential for NLRP3 inflammasome activity. This study aims find whether TXNIP/NLRP3 pathway dementia. According our studies on...
Introduction: SARS-CoV-2 causes various neurological sequelae in COVID-19 survivors including fatigue and cognitive dysfunction. Endothelial dysfunction, a key mechanism illness, is also major risk factor for vascular dementia (VaD). Clinical evidence suggests that reduced nitric oxide (NO) bioavailability likely pathogenic of endothelial dysfunction patients, eNOS levels decline with advancing age, both morbidity VaD . We hypothesize synthase (eNOS) deficiency contributes to brain infection...
Introduction: Ischemic stroke is a devastating brain injury and leading cause of mortality morbidity worldwide. Age the most influential co-morbidity, modulating severity, occurrence, cognitive impact. We have previously found that causes marked increase in cellular senescence senescence-associated secretory phenotype (SASP). In aged brain, cells develop into SASP which induces neuroinflammation further transform healthy cell to senescent (SC) via paracrine signaling. Although there baseline...
Objectives/Goals: SARS-CoV-2 infection has been shown to impact multiple organ systems, including the brain, and is associated with increased cognitive decline in vulnerable populations. The gut microbiome may play a significant role modulating these effects, as shifts microbiota composition have linked inflammation systemic disease processes. Methods/Study Population: To explore interactions, we conducted an acute COVID-19 study using 12-week-old C57 mice intranasally inoculated 1x10^4 PFU...
Abstract The novel coronavirus SARS-CoV-2 has caused significant global morbidity and mortality continues to burden patients with persisting neurological dysfunction. COVID-19 survivors develop debilitating symptoms include neuro-psychological dysfunction, termed “Long COVID”, which can cause reduction of quality life. Despite vigorous model development, the possible these underlying pathophysiology this devastating disease remains elusive. Mouse adapted (MA10) is a mouse-based simulates...