Our research activities focus on two major goals:
First, we investigate the long-term effects of early-life iron deficiency on the function of the limbic-hypothalamic pituitary adrenal (LHPA) axis.
Iron deficiency is a major global health concern that affects conservatively 2 billion individuals worldwide, including about 30% of pregnant women and pre-school age children. It is well established that early-life iron deficiency has long lasting negative effects on cognition and socio-emotional behaviors in humans despite prompt iron treatment following diagnosis. These long-term effects constitute a significant cost to society in terms of educational attainment, job potential, and mental health. Thus, we investigate how early-life iron deficiency alters cellular, molecular and epigenetic signatures in the developing brain using animal models. Insights into these fundamental alterations may lead to adjunctive therapies that can prevent and treat at risk pregnancies and children with iron deficiency.
Second, we investigate the biological role of a neural peptide (TMEM35/NACHO).
Recently, TMEM35 has been shown to function as a chaperone for nicotinic acetylcholine receptors (nAchRs), which have been implicated in neuropathologies and psychopathologies (e.g., addiction, pain, Autism, Alzheimer, and schizophrenia). Consistent with this finding, our investigation has shown that loss of TMEM35 function results in learning impairment, pain hypersensitivity, and increased risk for additive behaviors. Importantly, given the role of nAchRs in ischemic brain injury, we investigate their roles in the pathophysiology of neonatal hypoxia-ischemia brain injury. Understanding the precise molecular function of this novel peptide is promising in defining new mechanisms and pathways that regulate neuropathologies associated with nAchR dysregulation. These discoveries may lead to strategy to improving quality of life and productivity.