ÐÇ¿Õ´«Ã½

Dr. Chinyere Iweka obtained her B.Sc in Biology from the University of Maryland, Baltimore County, her M.Sc in Biotechnology from Johns Hopkins University and her Ph.D in Neuroscience from Georgetown University. Her previous research at the National Heart Lung and Blood Institute focused on identifying specific neuronal proteins that change their phosphorylation state in response to chondroitin sulfate proteoglycans (CSPGs), a sugar that is upregulated by reactive astrocytes in response to injury in the central nervous system (CNS). Using a phosphoproteomic screen, she identified phospholipid phosphatase-related protein 1 (PLPPR1), as a protein whose phosphorylation state changed in response to CSPGs to induce axon growth in neurons. Dr. Iweka discovered that PLPPR1 impedes the inhibitory activity of CSPGs and other inhibitory molecules such as lysophosphatidic acid, by modulating Rho-GTPases during CNS injury. During her postdoctoral training, Dr. Iweka focused on the non-neuronal responses to CNS injury – the peripheral immune cells that infiltrate the brain after injury. She became interested in how aging impacts immune function and the inflammatory response to stroke injury. She determined that there are age-dependent metabolic changes that correlate with the inflammatory response of monocytes/macrophages to stroke injury. These metabolic changes include changes in NAD+, a critical energy co-factor and modulator of immune function, also known to be impaired with aging.

Dr. Iweka’s future research will extend her findings to investigate the regulation of immune function and metabolism by the circadian clock in aging and age-related diseases. So far her studies show an age- dependent loss of circadian rhythmicity in macrophage trafficking and phagocytic function. She also determined that loss of the circadian clock protein, BMAL1 in microglia, the immune cell of the brain, resulted in reduced lysosomal activity that impacted their ability to prune synapses, resulting in increased synaptic density, impaired cognition and disruption of the sleep-wake cycle.