A5046216623- Neuroinflammation and Neurodegeneration Mechanisms
- Neuroscience and Neuropharmacology Research
- RNA regulation and disease
- Neurogenesis and neuroplasticity mechanisms
- Neurological Disease Mechanisms and Treatments
- Alzheimer's disease research and treatments
- S100 Proteins and Annexins
- Tryptophan and brain disorders
- Nanoparticles: synthesis and applications
- Mitochondrial Function and Pathology
- Nerve injury and regeneration
- Parkinson's Disease Mechanisms and Treatments
- Stress Responses and Cortisol
- Intensive Care Unit Cognitive Disorders
- Immune Response and Inflammation
- Neurological diseases and metabolism
- Nuclear Receptors and Signaling
- Adipose Tissue and Metabolism
- Atherosclerosis and Cardiovascular Diseases
- Gut microbiota and health
- Iron Metabolism and Disorders
- Barrier Structure and Function Studies
- Traumatic Brain Injury and Neurovascular Disturbances
- MicroRNA in disease regulation
- Paraquat toxicity studies and treatments
West Virginia University
2017-2024
Blanchette Rockefeller Neurosciences Institute
2019
Stanley Foundation
2013-2019
National Institute for Occupational Safety and Health
2000-2014
Centers for Disease Control and Prevention
2000-2014
Exponent (United States)
2009
University of South Florida
1997-2000
Florida College
1999
Pennsylvania State University
1992-1994
Penn State Milton S. Hershey Medical Center
1992-1994
Recessively inherited loss-of-function mutations in the PTEN-induced putative kinase 1(Pink1), DJ-1 (Park7) and Parkin (Park2) genes are linked to familial cases of early-onset Parkinson's disease (PD). As part its strategy provide more tools for research community, The Michael J. Fox Foundation Research (MJFF) funded generation novel rat models with targeted disruption ofPink1, or determined if loss these proteins would result a progressive PD-like phenotype. Pathological, neurochemical...
The pathogenic mechanisms underlying idiopathic Parkinson's disease (PD) remain enigmatic. Recent findings suggest that inflammatory processes are associated with several neurodegenerative disorders, including PD. Enhanced expression of the proinflammatory cytokine, tumor necrosis factor (TNF)-alpha, has been found in association glial cells substantia nigra patients To determine potential role for TNF-alpha PD, we examined effects 1-methyl-4-phenyl-1,2,3,4-tetrahydropyridine (MPTP), a...
Reactive gliosis is a hallmark of disease-, trauma-, and chemical-induced damage to the central nervous system. The signaling pathways associated with this response neural injury remain be elucidated, but recent evidence implicates Janus kinase (JAK)-signal transducer activator transcription (STAT) pathway. Here, we used known dopaminergic neurotoxicant, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), selectively striatal nerve terminals elicit glial response. We then analyzed changes...
Abstract Iron is necessary for normal neural function but it must be stringently regulated to avoid iron‐induced oxidative injury. The regulation of systeimic iron through the proteins transferrin (iron mobilization) and ferritin sequestration). This study examines cellular regional distribution iron‐related in selected regions adult aged rat brain. information a prerequisite understanding mechanism by which homeostasis maintained predominant cell type containing ferritin, transferrin,...
Enhanced expression of tumor necrosis factor (TNF) -alpha, is associated with the neuropathological effects underlying disease-, trauma- and chemically induced neurodegeneration. Previously, we have shown that deficiency TNF receptors protects against MPTP-induced striatal dopaminergic neurotoxicity, findings suggestive a role for TNF-alpha in Here, demonstrate suppresses microglial activation alters susceptibility brain regions to MPTP. microglia-derived factors, TNF-alpha, MCP-1,...
Abstract Ferritin is the major iron storage protein and accounts for majority of in brain. Thus, ferritin a key component protecting brain from induced oxidative damage. The high lipid content, rate metabolism, content combine to make organ most susceptible stress. role damage disruption homeostasis considered clinically important normal aging potential pathogenic number neurologic disorders including Alzheimer's disease Parkinson's disease. Little known, however, mechanism by which...
Abstract Engineered carbon nanotubes are newly emerging manufactured particles with potential applications in electronics, computers, aerospace, and medicine. The low density small size of these biologically persistent makes respiratory exposures to workers likely during the production or use commercial products. narrow diameter great length single‐walled (SWCNT) suggest interact critical biological structures. To examine induce genetic damage normal lung cells, cultured primary immortalized...
Abstract Carbon nanotubes are commercially-important products of nanotechnology; however, their low density and small size makes carbon nanotube respiratory exposures likely during production or processing. We have previously shown mitotic spindle aberrations in cultured primary immortalized human airway epithelial cells exposed to single-walled (SWCNT). In this study, we examined whether multi-walled (MWCNT) cause damage at doses equivalent 34 years exposure the NIOSH Recommended Exposure...
Mitochondrial dysfunction is thought to play a significant role in neurodegeneration observed Parkinson's disease (PD), yet the mechanisms underlying this pathology remain unclear. Here, we demonstrate that loss of mitoNEET (CISD1), an iron-sulfur containing protein regulates mitochondrial bioenergetics, results and striatal dopamine tyrosine hydroxylase. Mitochondria isolated from mice lacking were dysfunctional as revealed by elevated reactive oxygen species (ROS) reduced capacity produce...
Ischemic stroke is one of the leading causes morbidity and mortality. Treatment options are limited only a minority patients receive acute interventions. Understanding mechanisms that mediate neuronal injury death may identify targets for neuroprotective treatments. Here we show aberrant activity protein kinase Cdk5 principal cause in rodents during stroke. Ischemia induced either by embolic middle cerebral artery occlusion (MCAO) <i>in vivo</i> or oxygen glucose deprivation brain slices...
Motor learning and neuro-adaptations to drugs of abuse rely upon neuronal signaling in the striatum. Cyclin-dependent kinase 5 (Cdk5) regulates striatal dopamine neurotransmission behavioral responses cocaine. Although role for Cdk5 neurodegeneration cortex hippocampus hippocampal-dependent has been demonstrated, its dysregulation striatum not examined. Here we show that strong activation NMDA receptors produced p25, truncated form co-activator p35. Furthermore, inducible overexpression p25...