Christopher A. McPherson

ORCID: 0000-0002-6032-0853
Publications
Citations
Views
---
Saved
---
About
Contact & Profiles
Research Areas
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Immune Response and Inflammation
  • Immune cells in cancer
  • Anesthesia and Neurotoxicity Research
  • Neurogenesis and neuroplasticity mechanisms
  • Marine Biology and Environmental Chemistry
  • Neurological Disease Mechanisms and Treatments
  • Environmental Toxicology and Ecotoxicology
  • Genetics, Aging, and Longevity in Model Organisms
  • S100 Proteins and Annexins
  • Alzheimer's disease research and treatments
  • Cholinesterase and Neurodegenerative Diseases
  • Neonatal and fetal brain pathology
  • NF-κB Signaling Pathways
  • Pesticide Exposure and Toxicity
  • Mercury impact and mitigation studies
  • Heavy Metal Exposure and Toxicity
  • MicroRNA in disease regulation
  • Immune responses and vaccinations
  • Retinoids in leukemia and cellular processes
  • Trace Elements in Health
  • Heme Oxygenase-1 and Carbon Monoxide
  • Barrier Structure and Function Studies
  • Complementary and Alternative Medicine Studies
  • Osteoarthritis Treatment and Mechanisms

National Institutes of Health
2008-2024

National Institute of Environmental Health Sciences
2013-2024

University of North Carolina at Chapel Hill
2010-2011

Triangle
2002-2009

The sporadic nature of Alzheimer's disease (AD) argues for an environmental link that may drive AD pathogenesis; however, the triggering factors and period their action are unknown. Recent studies in rodents have shown exposure to lead (Pb) during brain development predetermined expression regulation amyloid precursor protein (APP) its amyloidogenic beta-amyloid (Abeta) product old age. Here, we report AD-related genes [APP, BACE1 (beta-site APP cleaving enzyme 1)] as well transcriptional...

10.1523/jneurosci.4405-07.2008 article EN cc-by-nc-sa Journal of Neuroscience 2008-01-02

Localized tumor necrosis factor-alpha (TNFalpha) elevation has diverse effects in brain injury often attributed to signaling via TNFp55 or TNFp75 receptors. Both dentate granule cells and CA pyramidal express TNF receptors (TNFR) at low levels a punctate pattern. Using model induce selective death of (trimethyltin; 2 mg/kg, i.p.), neuronal apoptosis [terminal deoxynucleotidyl transferase-mediated dUTP-biotin situ end labeling, active caspase 3 (AC3)] was accompanied by amoeboid microglia...

10.1111/j.1471-4159.2008.05382.x article EN Journal of Neurochemistry 2008-03-27

At elevated levels, fluoride (F−) exposure has been associated with adverse human health effects. In rodents, F− reported to induce deficits in motor performance and learning memory. this study, we examined Long-Evans hooded male rats maintained on a standard diet (20.5 ppm F−) or low (3.24 drinking water 0, 10, 20 from gestational day 6 through adulthood. postnatal 25, brain levels were 0.048 0.081 μg/g femur 235 379.8 for 10 F−, respectively. Levels increase age adults, plasma 0.036 0.025...

10.1007/s12640-018-9870-x article EN cc-by Neurotoxicity Research 2018-02-05

Alzheimer's disease (AD) is characterized by plaques of amyloid-β (Aβ) peptide, cleaved from protein precursor (AβPP). Our hypothesis that lifespan profiles AD-associated mRNA and levels in monkeys would differ mice t

10.3233/jad-2009-1138 article EN Journal of Alzheimer s Disease 2009-07-29

Abstract Microglia function as the tissue‐specific resident macrophages of nervous system, performing immune and non‐immune functions. These functions are critical to development maintain homeostasis in system throughout lifespan, during brain injury or disease. One method by which microglia is phagocytosis aberrant proteins, extracellular debris, synapses, apoptotic cells. Phagocytic can be changed environmental genetic risk factors that affect microglia. protocols present a rapid simple...

10.1002/cpz1.638 article EN Current Protocols 2023-01-01
Coming Soon ...