Postdoctoral Fellow

Neurobiology
National Institute of Neurological Disorders and Stroke, NIH
2000

Postdoctoral Fellow

Neurobiology
Harvard Medical School
1998

Doctor of Philosophy (Ph.D.)

Physiology (Neurophysiology)
Meharry Medical College
1995

Bachelor of Science (B.S.)

Biology
Grambling State University
1989

Anatomy

Cerebral Circulation and Blood Supply

Interdisciplinary Biomedical Science

Alpha Omega Alpha Medical Honor Society Inductee, 2024

INSIGHT Into Diversity 2020 Inspiring Programs in STEM Award (B2B Program), 2020

Harold D. West, Ph.D. Distinguished Biomedical Scientist Award, Meharry Medical College, 2013

Book Chapters

Chapter 28: Gene Interaction Hierarchy Analysis Can Be an Effective Tool for Managing Big Data Related to Unilateral Traumatic Brain Injury in Brain Neurotrauma: Molecular, Neuropsychological, and Rehabilitation Aspects

This chapter discusses the utility of gene interaction hierarchy (GIH) analysis for the management of large datasets. This step-wise analysis combines Ingenuity Pathways Analysis (IPA®) with other offline techniques to identify genes that are central to gene expression patterns in the data. Specifically, this example uses IPA®’s functional analysis capabilities to identify genes that are associated with cell growth and proliferation (CGP) following unilateral traumatic brain injury (TBI).

Neuregulin-1 promotes early regenerative and autophagic responses after ischemic stroke via spatial proteomics

Neuregulin-1 promotes early regenerative and autophagic responses after ischemic stroke via spatial proteomics

Ischemic stroke remains a leading cause of death and long-term disability, yet effective treatments that promote recovery beyond the acute phase are lacking. Neuregulin-1 (NRG-1) has shown potent neuroprotective and anti-inflammatory properties in preclinical stroke models, with evidence of enhanced neuronal regeneration when administered after injury. To investigate the spatial mechanisms underlying its neuroregenerative therapeutic effects, we examined brain proteomic responses to post-ischemic NRG-1 treatment in mice using NanoString Digital Spatial Profiling (DSP).

Transcriptomic identification of CREB1 and FOXO1 activation in neuregulin-1-mediated neuroprotection after stroke

Transcriptomic identification of CREB1 and FOXO1 activation in neuregulin-1-mediated neuroprotection after stroke

Neuregulin-1 (NRG-1) is a growth factor that has been investigated for its neuroprotective properties following ischemic stroke. While NRG-1 has shown considerable promise in reducing neuronal damage, the molecular mechanisms underlying its protective effects remain unclear. This study aimed to examine the impact of NRG-1 treatment on ischemia-induced gene expression following permanent middle cerebral artery occlusion (MCAO) in rats.

Redox State of Glutathione and Cysteine in Plasma Following Acute Stroke

Redox State of Glutathione and Cysteine in Plasma Following Acute Stroke

Ischemic stroke is a major cause of long-term disability and death, with oxidative stress contributing substantially to post-ischemic injury. Reperfusion restores oxygen supply but simultaneously increases reactive oxygen species (ROS), amplifying secondary neuronal damage. This study examined time-dependent changes in systemic thiol redox status following transient middle cerebral artery occlusion (tMCAO) in rats. Plasma concentrations of cysteine (CySH), cystine (CySS), glutathione (GSH), and glutathione disulfide (GSSG), along with corresponding CySS/CySH and GSSG/GSH ratios and redox potentials (Eh), were evaluated 24 and 48 h after occlusion. At 24 h, thiol concentrations and redox ratios showed no significant differences between sham and tMCAO groups. By 48 h, a marked oxidative shift emerged, characterized by reduced CySH, elevated GSSG, and significant increases in both CySS/CySH and GSSG/GSH ratios. Redox potentials also demonstrated substantial oxidation at this time point. These findings indicate that prolonged ischemia–reperfusion induces systemic oxidative stress, with plasma redox status serving as a sensitive indicator of reperfusion-related injury. The results underscore the plasma redox status as a potentially sensitive biomarker of reperfusion-induced oxidative injury and support the therapeutic value of targeting redox imbalance to mitigate oxidative damage following stroke.

Toxoplasma infection induces an aged neutrophil population in the CNS that is associated with neuronal protection

Toxoplasma infection induces an aged neutrophil population in the CNS that is associated with neuronal protection

Infection with the protozoan parasite Toxoplasma gondii leads to the formation of lifelong cysts in neurons that can have devastating consequences in the immunocompromised. In the immunocompetent individual, anti-parasitic effector mechanisms and a balanced immune response characterized by pro- and anti-inflammatory cytokine production establishes an asymptomatic infection that rarely leads to neurological symptoms. Several mechanisms are known to play a role in this successful immune response in the brain including T cell production of IFNγ and IL-10 and the involvement of CNS resident cells. This limitation of clinical neuropathology during chronic infection suggests a balance between immune response and neuroprotective mechanisms that collectively prevent clinical manifestations of disease. However, how these two vital mechanisms of protection interact during chronic Toxoplasma infection remains poorly understood.

The case for neuregulin-1 as a clinical treatment for stroke

The case for neuregulin-1 as a clinical treatment for stroke

Ischemic stroke is the leading cause of serious long-term disability and the 5th leading cause of death in the United States. Revascularization of the occluded cerebral artery, either by thrombolysis or endovascular thrombectomy, is the only effective, clinically-approved stroke therapy. Several potentially neuroprotective agents, including glutamate antagonists, anti-inflammatory compounds and free radical scavenging agents were shown to be effective neuroprotectants in preclinical animal models of brain ischemia. However, these compounds did not demonstrate efficacy in clinical trials with human patients following stroke. Proposed reasons for the translational failure include an insufficient understanding on the cellular and molecular pathophysiology of ischemic stroke, lack of alignment between preclinical and clinical studies and inappropriate design of clinical trials based on the preclinical findings. Therefore, novel neuroprotective treatments must be developed based on a clearer understanding of the complex spatiotemporal mechanisms of ischemic stroke and with proper clinical trial design based on the preclinical findings from specific animal models of stroke. We and others have demonstrated the clinical potential for neuregulin-1 (NRG-1) in preclinical stroke studies. NRG-1 significantly reduced ischemia-induced neuronal death, neuroinflammation and oxidative stress in rodent stroke models with a therapeutic window of >13 h. Clinically, NRG-1 was shown to be safe in human patients and improved cardiac function in multisite phase II studies for heart failure. This review summarizes previous stroke clinical candidates and provides evidence that NRG-1 represents a novel, safe, neuroprotective strategy that has potential therapeutic value in treating individuals after acute ischemic stroke.