Date of Award

Spring 2021

Document Type

Open Access Dissertation



First Advisor

Rosemarie Booze


HIV is a serious viral infection that persists in the brain despite treatment. Approximately half of all seropositive patients will experience some degree of comorbid depression, as well as HIV associated neurocognitive disorders. The present research sought to evaluate the therapeutic efficacy of escitalopram, a selective serotonin reuptake inhibitor in ameliorating neuroanatomical and biochemical markers associated with HIV infection. The central purpose of this research is to characterize the effects of escitalopram treatment upon dendritic spine proliferation in the nucleus accumbens. Previous research has consistently demonstrated impaired synaptodendritic integrity in this region, with underlying mechanisms remaining unclear. A secondary focus of the proposed research was to quantify telomere length in the HIV-1 transgenic rat treated with escitalopram. Finally, neurogenesis in the hippocampus was examined using immunohistochemical methods. Escitalopram successfully reversed HIV-1 mediated synaptodendritic damage in the nucleus accumbens. HIV-1 rats treated with escitalopram exhibited population shifts in spine morphology and increased dendritic branching. However, escitalopram did not appear to be successful at promoting neurogenesis and likewise did not produce an increase in telomere length as quantified by qPCR. Collectively, these findings illustrate the therapeutic potential of escitalopram in treating HIV-1 associated synaptic damage but suggest that further research in the potential treatment is necessary.

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