Chinyere Agbaegbu Iweka, Ph.D.

Postdoctoral Fellow, Stanford University
Chinyere Agbaegbu Iweka headshot

Chinyere Agbaegbu Iweka is a postdoctoral fellow in the lab of Katrin Andreasson in the Department of Neurology at the Stanford University School of Medicine. Agbaegbu Iweka obtained her bachelor’s degree in biology from the University of Maryland, Baltimore County, and her master’s degree in biotechnology from Johns Hopkins University. She earned her doctorate in neuroscience from Georgetown University where she investigated the mechanisms underlying neuronal responses to inhibitory factors upregulated in response to injury to the central nervous system.

During her postdoctoral training, Agbaegbu Iweka became interested in understanding how neuron-immune cell interactions are affected by aging and disease. She began by investigating the circadian rhythms of immune cells, known to decline significantly with age. She discovered that the loss of the circadian clock through deletion of the clock protein, BMAL1, in microglia accelerates age-related cognitive decline, decreases hippocampal synaptic plasticity, and disrupts the sleep-wake cycle by a mechanism involving defective synaptic pruning.

Agbaegbu Iweka is a recipient of several awards including the Burroughs Wellcome Postdoctoral Diversity Enrichment program award (2022–2025), the Stanford JumpStart award (2020–2021), and the SUMS Seed Grant (2019–2020). For her work in promoting diversity, equity and inclusion at Stanford, she was presented with the inaugural Stanford Postdoc JEDI Award (2021).

Project: Circadian regulation of immune cell metabolism and the effect on cognitive flexibility in the aging brain

A hallmark of aging is “inflammaging,” a chronic low-grade inflammatory state that persists without cause and is strongly linked to cognitive decline. Immune cells have diverse functions that require distinct metabolic demands in order to attain sufficient energy for effective host defense and tissue homeostasis.However, metabolic function significantly declines with aging. Both metabolism and immune function are regulated by the circadian clock. The circadian clock functions to temporally synchronize all physiological mechanisms within an organism with the external light/dark cycle to maintain homeostasis in a changing environment. Repeated disruption of the circadian clock through aging, shift-work and jet-lag adversely impacts health leading to metabolic disorders, including cognitive decline. However, the metabolic mechanisms under circadian control that direct age-related maladaptive immune function and contribute to cognitive decline remain unexplored. My research proposal will address the following questions: 1) What specific clock-controlled metabolic pathways underlie age-related inflammation and cognitive deficits? 2) Would restoring metabolic components such as NAD+ in immune cells reduce age-related inflammation and improve cognitive aging? My research program will provide a deeper understanding of the clock-dependent mechanisms that regulate immune cell metabolism and function and investigate how imbalances in these systems promote cognitive decline in aged individuals.

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