MarketSusan Ackerman (neuroscientist)
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Susan Ackerman (neuroscientist)

Susan L. Ackerman is an American neuroscientist and geneticist. Her work has highlighted some of the genetic and biochemical factors that are involved in the development of the central nervous system and age-related neurodegeneration. Her research is aimed at helping scientists understand what causes several types of neurodegeneration in mammals. This research, and others' like it, may lead to cures for neurodegenerative diseases. Ackerman is a professor at University of California, San Diego. She was formerly a professor at the Jackson Laboratory and the Sackler School of Graduate Biomedical Sciences at Tufts University. She also serves as an adjunct professor at the University of Maine, Orono. Ackerman was an associate geneticist at Massachusetts General Hospital in Boston, Massachusetts.

Education
As an undergraduate, Ackerman attended California State University (Chico), graduating with a Bachelor of Arts degree in Chemistry, and a Bachelor of Arts degree in Biology. Subsequently, Ackerman pursued graduate studies, earning a Doctorate in Biology at the UCLA. == Career and research ==
Career and research
Since 2005, Ackerman has served as an investigator at the Howard Hughes Medical Institute. In her lab, she focuses on determining how neurological homeostasis in developed and aging brains is linked to molecular pathways. Through phenotype-driven forward genetics and gene-driven reverse genetics, she identifies mutations which lead to abnormal CNS development or neurodegeneration, uncovering pathways which are not typically related to loss of neural function or human disease. and to the National Academy of Medicine in 2020. Unc5c Ackerman's research has centered largely on the Unc5c gene. Her research on Unc5c protein revealed that the protein is integral in the development of the corpus callosum, the neurons that form the connection between the two hemispheres of the brain. A mutation in the Unc5c gene, in association with other mutated genes, leads to a degeneration of the corpus callosum. However, if Unc5c is the only gene that is mutated, no noticeable difference in the corpus callosum is present. This is because the Unc5c receptor is only integral in the formation of the corpus callosum in early-born, deep layer neurons. These neurons comprise a small percentage of the corpus callosum relative to the late-born, upper layer neurons. Other research Other projects Ackerman has been involved in include the mutation of a U2 snRNA and its connection to neurodegeneration, an editing defective tRNA synthetase that leads to protein misfolding and neurodegeneration, and ribosome stalling by tRNA mutations that leads to neurodegeneration. == References ==
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