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IMPAIRED BRIDGING OF TEMPORAL DISCONTINUITIES IN OLDER ADULT HIV-1 TG RATS.

Kristen A McLaurin1,2, Hailong Li1, Allison Ritchie1

  • 1Program in Behavioral Neuroscience, Department of Psychology, Barnwell College, University of South Carolina 1512 Pendleton Street, Columbia, SC 29208.

Biorxiv : the Preprint Server for Biology
|April 17, 2026
PubMed
Summary
This summary is machine-generated.

The HIV-1 transgenic rat model shows age-related neurocognitive impairments and neuronal dysfunction, offering a new system to study human immunodeficiency virus type 1 (HIV-1) effects on the aging brain.

Keywords:
Amyloid BetaAttentionDendritic SpinesNeurocognition

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Area of Science:

  • Neuroscience
  • Virology
  • Gerontology

Background:

  • Combination antiretroviral therapy has increased the lifespan of individuals with human immunodeficiency virus type 1 (HIV-1), leading to a growing population of older adults living with HIV-1.
  • Age-related neurocognitive impairments are a significant concern in aging HIV-1 populations, yet a suitable in vivo model is lacking.
  • Understanding the mechanisms behind these impairments is crucial for developing effective interventions.

Purpose of the Study:

  • To evaluate the utility of the HIV-1 transgenic (Tg) rat as a biological system for modeling age-related neurocognitive impairments and neuroanatomical alterations.
  • To investigate the specific neurocognitive deficits and underlying neuronal dysfunction in older HIV-1 Tg rodents.

Main Methods:

  • Utilized older adult HIV-1 Tg rats (>12 months of age) and age-matched control counterparts.
  • Assessed neurocognitive function through tests measuring stimulus-reinforcement learning, sustained attention, and selective attention.
  • Examined neuronal structure, dendritic spine morphology in the medial prefrontal cortex, and amyloid beta (Aβ) accumulation.

Main Results:

  • Older HIV-1 Tg rats exhibited profound neurocognitive impairments, including deficits in learning, sustained attention, and selective attention, suggesting temporal processing distortions.
  • Neuronal dysfunction was evident, characterized by structural alterations in pyramidal neurons and dendritic spines in the medial prefrontal cortex, along with abnormal Aβ accumulation.
  • Amyloid beta accumulation partially explained dendritic spine dysmorphology in male HIV-1 Tg rats, while neuronal dysfunction was a primary driver of neurocognitive impairments in both sexes.

Conclusions:

  • The HIV-1 Tg rat serves as a valuable in vivo model for studying age-related neurocognitive impairments associated with HIV-1.
  • Neuronal dysfunction, driven by HIV-1 proteins, is a key mechanism underlying neurocognitive deficits in aging HIV-1 populations.
  • This model facilitates research into the roles of HIV-1, aging, and comorbidities in neurocognitive decline.