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HIV-1 gp120 Impairs Spatial Memory Through Cyclic AMP Response Element-Binding Protein.

Jenny Shrestha^1,2, Maryline Santerre^1,2, Charles N S Allen^1,2

¹Molecular Studies of Neurodegenerative Diseases Lab, Philadelphia, PA, United States.

Frontiers in Aging Neuroscience

|May 26, 2022

Summary

HIV-gp120 protein impairs brain function by disrupting cellular energy and mitochondria, leading to neurocognitive disorders. Inhibiting PDE4 with rolipram may restore function by preserving CREB protein activity.

Keywords:

CREB protein HIV mitochondria neurodegeneration rolipram

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Development of Cell-type specific anti-HIV gp120 aptamers for siRNA delivery

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Area of Science:

Neuroscience
Molecular Biology
Virology

Background:

HIV-associated neurocognitive disorders (HAND) persist despite antiretroviral therapy.
The HIV-gp120 protein is implicated in neurodegeneration.
Mechanisms linking gp120 to neuronal dysfunction require elucidation.

Purpose of the Study:

To investigate the role of HIV-gp120 protein in neurodegeneration.
To identify the molecular mechanisms by which gp120 affects neuronal function.
To explore potential therapeutic targets for HAND.

Main Methods:

In vitro and in vivo studies using cell cultures and animal models.
Analysis of cellular metabolism, mitochondrial function, and synaptic plasticity.
Investigation of signaling pathways involving CREB, PGC1α, and BDNF.
Pharmacological intervention with rolipram, a PDE4 inhibitor.

Main Results:

HIV-gp120 induces neurodegeneration via metabolic reprogramming, decreasing ATP levels and mitochondrial integrity.
gp120 disrupts mitochondrial dynamics and synaptic plasticity.
gp120 inhibits CREB phosphorylation at serine 133, leading to reduced PGC1α and BDNF expression.
Rolipram treatment restored CREB phosphorylation and alleviated gp120-induced deficits.

Conclusions:

HIV-gp120 protein contributes to HAND by inhibiting CREB protein function.
Targeting the PDE4 pathway may offer a therapeutic strategy for HAND.