Posters
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Staff
Academic/Professional Position (Other)
Research Associate
Academic Level (Author 1)
Staff
Discipline/Specialty (Author 1)
Neuroscience
Academic Level (Author 2)
Post-doc
Discipline/Specialty (Author 2)
Neuroscience
Academic Level (Author 3)
Medical Student
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Medical Student
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Medical Student
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Poster
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Community/Public Health
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Research/Clinical
Abstract
Background: AD is a devastating neurodegenerative disorder and one of the most common causes of neurodegenerative dementia. AD is characterized by a progressive impairment of cognitive functions. Prominent pathophysiological characteristics of AD include extracellular amyloid β (Aβ) plaques and intracellular neurofibrillary tangles (NFTs) composed of hyperphosphorylated tau (p-tau) proteins. An estimated 6.9 million Americans aged 65 and older are living with AD today. This number could grow to 13.8 million by 2060 barring the development of medical breakthroughs to prevent or cure AD. According to the Centers for Disease Control and Prevention (CDC), roughly 53% of American adults living with HIV are over the age of 50, due mainly to the successful treatment regimens helping HIV-positive adults survive for decades with HIV. Aging is the primary risk factor for AD and 53% of American adults living with HIV are over the age of 50. As the population ages, the number of individuals who experience AD and HIV will also increase, and therefore, the comorbidity of these two clinically unmet is unavoidable.
Methods: We will use the chimeric HIV (EcoHIV) model. This model consists of injecting conventional mice with EcoHIV, which uses species-specific cellular receptors to enter mouse cells. We tested the animals for cognitive decline using NOR every week for several weeks. The NOR was performed in an open field box. NOR relies on rodents' natural proclivity for exploring novelty. NOR task performance is quantified using the Recognition Index (RI) = Time(novel)/[time(novel) + time(familiar) x100.
Results: EcoHIV promotes the onset of cognitive decline in Tau mice at 5 weeks post- EcoHIV cognitive. A) The baseline of cognitive function of Tau and WT mice before EcoHIV infection. B) The lack of effect of EcoHIV on Tau mice cognition function using NOR at 2 weeks post-EcoHIV. C) EcoHIV promotes the cognitive decline of Tau mice using NOR at 5 weeks post- EcoHIV. Data are represented as mean ± SEM. ns; not significant. * p<0.05. RI; Recognition Index. EcoHIV promotes the onset of cognitive decline in KI mice at 11 weeks post- EcoHIV cognitive.
Conclusion: These data provide the first evidence for an in vivo functional interaction between EcoHIV and two AD mouse models.
Also presented as an Oral Presentation.
Recommended Citation
Rios, Jose; Alnoud, Mohammed; Franco, Emmanuel; Mills, Justin D.; Nwose, Joshua; Malbas, Maria Sophia; Garcia, Hiram L.; and Benamar, Khalid, "Alzheimer’s disease and HIV-1 comorbidity" (2025). Research Symposium. 187.
https://scholarworks.utrgv.edu/somrs/2025/posters/187
Included in
Alzheimer’s disease and HIV-1 comorbidity
Background: AD is a devastating neurodegenerative disorder and one of the most common causes of neurodegenerative dementia. AD is characterized by a progressive impairment of cognitive functions. Prominent pathophysiological characteristics of AD include extracellular amyloid β (Aβ) plaques and intracellular neurofibrillary tangles (NFTs) composed of hyperphosphorylated tau (p-tau) proteins. An estimated 6.9 million Americans aged 65 and older are living with AD today. This number could grow to 13.8 million by 2060 barring the development of medical breakthroughs to prevent or cure AD. According to the Centers for Disease Control and Prevention (CDC), roughly 53% of American adults living with HIV are over the age of 50, due mainly to the successful treatment regimens helping HIV-positive adults survive for decades with HIV. Aging is the primary risk factor for AD and 53% of American adults living with HIV are over the age of 50. As the population ages, the number of individuals who experience AD and HIV will also increase, and therefore, the comorbidity of these two clinically unmet is unavoidable.
Methods: We will use the chimeric HIV (EcoHIV) model. This model consists of injecting conventional mice with EcoHIV, which uses species-specific cellular receptors to enter mouse cells. We tested the animals for cognitive decline using NOR every week for several weeks. The NOR was performed in an open field box. NOR relies on rodents' natural proclivity for exploring novelty. NOR task performance is quantified using the Recognition Index (RI) = Time(novel)/[time(novel) + time(familiar) x100.
Results: EcoHIV promotes the onset of cognitive decline in Tau mice at 5 weeks post- EcoHIV cognitive. A) The baseline of cognitive function of Tau and WT mice before EcoHIV infection. B) The lack of effect of EcoHIV on Tau mice cognition function using NOR at 2 weeks post-EcoHIV. C) EcoHIV promotes the cognitive decline of Tau mice using NOR at 5 weeks post- EcoHIV. Data are represented as mean ± SEM. ns; not significant. * p<0.05. RI; Recognition Index. EcoHIV promotes the onset of cognitive decline in KI mice at 11 weeks post- EcoHIV cognitive.
Conclusion: These data provide the first evidence for an in vivo functional interaction between EcoHIV and two AD mouse models.
Also presented as an Oral Presentation.
