Reduction in Zinc Neurotransmission Induces Neurodegeneration


Guadalupe Martinez, Emily Vogler


Jorge Busciglio, Associate Professor, Neurobiology and Behavior, University of California Irvine

Alzheimer’s disease is a progressive neurodegenerative disease for which there is presently no cure. It is the 6th leading cause of death in the United States, costing the nation $203 billion in the year 2013 alone. This research project was conducted in order to better understand the role of zinc as a neurotransmitter in Alzheimer’s disease pathology and for acquisition of further knowledge. Brain sections of two and thirteen month old wild type mice and ZnT3-/- transgenic (mice lacking the ability to use zinc as a neurotransmitter) mice were labeled with DAPI to stain for nuclei and Fluoro-Jade C to stain for degenerating neurons. The superimposition of these two stains verifies the presence of a degenerating neuron. The number of degenerating neurons was then counted and a comparison was carried out between the different ages and genotypes of mice. Results indicate that there is increased neurodegeneration in the CA3 region of the hippocampus of ZnT3-/- mice compared to the wild type due to the lack of synaptic zinc in the mossy fiber terminals in that region. These results provide evidence that a lack, or dysregulation, of zinc plays an important role in the onset and/or progression of Alzheimer’s disease. These results would further implicate and highlight the importance of zinc in the pathology of Alzheimer’s disease and also possibly lead to novel research directions involving the regulation of zinc.

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Saturday, November 23, 2013




Poster Session 2 - Villalobos Hall

Presentation Type:

Poster Presentation