Richard E. Hartman, PhD

I graduated from Missouri State University in 1993 with a BS in experimental psychology. I then enrolled in the Behavior, Brain & Cognition program at Washington University in St. Louis, where I studied rodent behavior and neurodegeneration under behavioral expert Dave Wozniak in John Olney’s lab. During this time, I helped Dave set up Washington University’s Animal Behavior Core facility. I defended my PhD dissertation (on the long-term cognitive effects of ischemic stroke in rats) on September 11, 2001, then did a 4-year postdoctoral fellowship in the lab of Alzheimer’s disease guru Dave Holtzman. While in the Holtzman lab, I worked with a number of transgenic and knockout mouse models of Alzheimer’s disease and learned biochemical/histological techniques for assessing biomarkers of neuropathology. I have been publishing papers characterizing rodent behavioral phenotypes since 2001. My first paper characterizing neuropathology following brain injury used a mouse model of traumatic brain injury. Since then, I have published papers characterizing brain injury resulting from early drug exposure, global ischemia, intracerebral hemorrhage, and impact trauma, as well as characterizing a number of transgenic mouse lines and neuroprotective strategies.

The Hartman behavioral neuroscience lab at Loma Linda University in southern California primarily uses animal models (rats, transgenic/ knockout mice, and drosophila melanogaster [fruit flies]) of neurological disease to understand their mechanisms and potential therapeutic treatments. Techniques used include behavioral assessment (e.g., water maze), psychopharmacology (e.g., manipulation of behavior with drugs), surgery (e.g., induction of stroke and/or traumatic brain injury), histology / immunohistochemistry (e.g., visualization of neurons, white matter, proteins, amyloid plaques, etc. in brain slices), stereological microscopy (unbiased quantification of brain structures under a microscope), and biochemistry (e.g., protein assays of brain tissue using Western blot, ELISA, etc.).

Long-standing collaborations and multiple intra- and extra-mural grants (LLU, NASA, NINDS, NICHD, DOD, NRSA, California Table Grape Commission) have yielded over 60 publications characterizing rodent models of juvenile and adult neurodegeneration (traumatic brain injury, stroke, radiation, exposure to anesthesia, Alzheimer’s disease) and treatments for these nervous system insults (e.g., monoclonal antibodies, polyphenols, stem cells, melatonin, osteopontin, fingomilod, MMP inhibition, DJNK inhibition, hemodilution, glucocorticoids, and aquaporin-4 RNA interference). We also function as the Neurobehavioral Core Facility for Loma Linda University’s Center for Brain Hemorrhage Research.

Our lab’s research is broadly concerned with promoting healthy brain aging / increasing an individual’s “health-span”, and generally falls into 1 of 3 overlapping categories: 1) Characterizing models of neurodegeneration, 2) Preventing neurodegeneration and/or increasing the brain’s resiliency, and 3) Characterizing the effects of plant-based compounds (phytochemicals) in the brain. Our main interests lie in exploring the interface between acute and/or chronic brain injury (e.g., TBI, stroke, radiation) and subsequent neurodegeneration (e.g., Alzheimer’s, chronic traumatic encephalopathy) and in dissecting the mechanisms by which phytochemicals (e.g., polyphenols) can influence the brain’s recovery and function under these conditions. Presumably, the beneficial effects of polyphenols (including the phenolic acids and flavonoids) are mediated by their ability to suppress inflammatory pathways and activate antioxidant pathways.

We have shown that traumatic brain injury can accelerate the development of Alzheimer’s- like neuropathology in rodents (Hartman, et al., 2002; Pop, et al., 2012) and that preventing accumulation of amyloid plaques in their brains with a monoclonal antibody or dietary phytochemicals can prevent the age-related decline in cognition seen in these animals (Hartman, et al., 2005; Hartman, et al., 2006). Interestingly, dietary supplementation with pomegranate juice reduced soluble amyloid-β and plaques by ~50% in the brains of transgenic mice, and this was associated with significantly improved cognitive and physical performance. More importantly, we have shown that administering pomegranate-derived polyphenols improved cognitive and physical performance in humans after heart surgery (Ropacki, et al., 2013) and stroke (Bellone, et al., 2018). Other experimental data from our lab demonstrates that pomegranate supplementation protected against depression-like behaviors (learned helplessness) induced by radiation exposure (Dulcich & Hartman, 2013) and improved swim speed in transgenic mice (Hartman, et al., 2006). Another phytochemical (resveratrol) was found to improve behavior and neuropathology associated with subarachnoid hemorrhage in rats (Wan, et al., 2018).