Alzheimer’s disease (AD) is a devastating neurodegenerative disease characterized by the accumulation of amyloid beta (Aβ) peptides within the brain. The buildup of amyloid plaques in the AD brain disrupts synaptic functions, leading to progressive neuronal degeneration, culminating in the death of the AD patient within ten years of diagnosis. As of writing this letter, no treatment exists that is capable of impeding AD progression. However, Dr. Carter’s hypothesis that increasing apolipoprotein E (ApoE) levels in the AD brain facilitates Aβ clearance and may eventually retard AD progression and possibly cure the disease. Having followed her career since she began her doctoral research at Case Western Reserve University, I can personally attest
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Carter’s experience includes a master’s degree in neuroscience from at Taiwan University. After completing her master’s, she worked as a research assistant for three years. In 2005, she gained admittance to Case Western Reserve University’s doctoral program. Dr. Carter’s Ph.D. research investigated the role of apolipoprotein E (ApoE) in proteolytic Aβ degradation. While the association between ApoE and Aβ is well established in AD research, the underlying pathology of this association remained largely unknown prior to Dr. Carter’s research. In an early study, Dr. Carter introduced ApoE into cultured microglia and astrocyte-conditioned media. Through comprehensive biochemical and cell-based analyses, she determined that the presence of ApoE facilitates both extracellular and intracellular Aβ clearance, revealing a previously unappreciated function of apolipoprotein. In the process assessing her findings, she invented a new biochemical method for quantitative analysis of Aβ clearance, which has since become a standard of AD …show more content…
Carter determined that sufficient ApoE lipidation status is necessary to stimulate Aβ degradation. She subsequently used mouse models of AD to demonstrate that pharmacologically inducing ApoE expression promotes Aβ degradation in the AD brain, a significant development in itself. In addition to facilitating Aβ clearance, Dr. Carter’s pharmaceutical treatment rapidly reversed cognitive deficits and restored social behavior in AD mice, a profound development regarding the future of AD treatment. Furthermore, Dr. Carter’s use Bexarotene, a drug already FDA-approved for treatment of T-cell lymphoma, to induce ApoE lipidation, permitted her unique treatment to forego redundant toxicity tests, entering directly into Phase II clinical trials at the University of Michigan Alzheimer’s Disease
Carter’s experience includes a master’s degree in neuroscience from at Taiwan University. After completing her master’s, she worked as a research assistant for three years. In 2005, she gained admittance to Case Western Reserve University’s doctoral program. Dr. Carter’s Ph.D. research investigated the role of apolipoprotein E (ApoE) in proteolytic Aβ degradation. While the association between ApoE and Aβ is well established in AD research, the underlying pathology of this association remained largely unknown prior to Dr. Carter’s research. In an early study, Dr. Carter introduced ApoE into cultured microglia and astrocyte-conditioned media. Through comprehensive biochemical and cell-based analyses, she determined that the presence of ApoE facilitates both extracellular and intracellular Aβ clearance, revealing a previously unappreciated function of apolipoprotein. In the process assessing her findings, she invented a new biochemical method for quantitative analysis of Aβ clearance, which has since become a standard of AD …show more content…
Carter determined that sufficient ApoE lipidation status is necessary to stimulate Aβ degradation. She subsequently used mouse models of AD to demonstrate that pharmacologically inducing ApoE expression promotes Aβ degradation in the AD brain, a significant development in itself. In addition to facilitating Aβ clearance, Dr. Carter’s pharmaceutical treatment rapidly reversed cognitive deficits and restored social behavior in AD mice, a profound development regarding the future of AD treatment. Furthermore, Dr. Carter’s use Bexarotene, a drug already FDA-approved for treatment of T-cell lymphoma, to induce ApoE lipidation, permitted her unique treatment to forego redundant toxicity tests, entering directly into Phase II clinical trials at the University of Michigan Alzheimer’s Disease