Gordon Ibeanu, Ph.D.
Associate Professor of Pharmaceutical Sciences
Molecular mechanisms and cellular targets of novel agents in Alzheimer’s disease PUBLICATIONS:
Neurodegenerative diseases such as Alzheimer’s disease (AD), Huntington’s disease (HD), and Parkinson’s disease (PD) are characterized by complex initiation of cellular abnormalities that lead to progressive neuronal cell damage and subsequent death of neurons. A considerable amount of in vitro and in vivo data has accumulated that demonstrate the proliferative and neuroprotective roles for nerve growth factor (NGF) and other neurotrophic factors in the survival and maintenance of neuronal cells. Despite the tremendous research focus on the role of amyloid beta in AD it is also likely that AD may in part result from inadequate NGF transmission. However, attempts to influence the disease progression with naturally occurring neurotrophic factors have failed to demonstrate efficacy due to factors inherent in peptide delivery across the blood brain barrier. Our goal is to develop and pharmacologically activate small molecule enhancers of NGF activity as tools to explore cellular targets and novel mechanisms of NGF actions in neurons. Promising compounds could potentially be developed for therapeutic intervention in the treatment of neurodegenerative diseases of the central nervous system.
G-protein coupled receptors as agents of human cancers.
G-protein coupled receptors (GPCR) are a diverse super family of heptahelical transmembrane proteins that tranduce information from surrounding environment to cells. They are activated by a wide range of bioactive molecules including peptides, hormones, lipids, growth factors, ions, odorants and photons. Activation of GPCRs alters the levels of intracellular second messenger systems by interacting with the trimeric guanine nucleotide binding proteins (G-proteins). Although many GPCR pathways linked to the dysregulation of pathophysiologic processes are well researched little is known on the role they play in the development and progression of cancers in humans. Evidence accumulated in the last couple of years strongly suggests the existence of a link between the regulation of GPCR functions and human tumors. We are interested in characterizing the role of a family of proton-sensing GPCR dependent pathways that lead to a poorly understood cycle of abnormal growth in target cells to understand the role of GPCRs in human cancer.