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Modeling Neuronal Death and Degeneration in Mouse Primary Cerebellar Granule Neurons
Published on: November 6, 2017
Neurobiological mediators of neuronal apoptosis in experimental neuroAIDS
M T Corasaniti1, D Rotiroti, G Nappi
1Department of Pharmacobiological Sciences, University of Catanzaro 'Magna Graecia', C/o Complesso Nini; Barbieri, 88021 Roccelletta di Borgia, Catanzaro, Italy. mtcorasa@unicz.it
Abstract:
Neuronal loss has often been described at post-mortem in the brain neocortex of patients suffering from AIDS. Neuroinvasive strains of HIV infect macrophages, microglial cells and multinucleated giant cells but not neurones. Processing of the virus by cells of the myelomonocytic lineage yields viral products that, in conjunction with potentially neurotoxic molecules generated by the host, might initiate a complex network of events which leads neurones to death. In particular, the HIV-1 coat glycoprotein gp120 has been proposed as a likely aetiologic agent of the described neuronal loss because it causes death of neurones in culture. More recently, it has been shown that brain neocortical cell death is caused in rat by intracerebroventricular injection of a recombinant gp120 coat protein and this occurs via apoptosis. The latter observation broadens our knowledge in the pathophysiology of the reported neuronal cell loss and opens a new lane of experimental research for the development of novel therapeutic strategies to limit damage to the brain of patients suffering from HIV associated dementia.
Insights
HIV-1
Area of Science:
- Neuroscience
- Virology
- Immunology
Background:
- Neuronal loss is a common finding in the brain neocortex of patients with Acquired Immunodeficiency Syndrome (AIDS).
- Human Immunodeficiency Virus (HIV) infects immune cells, not neurons directly, but viral products may trigger neuronal death.
- The HIV-1 coat glycoprotein gp120 is a suspected cause of this neuronal loss.
Purpose of the Study:
- To investigate the role of HIV-1 gp120 in causing neuronal cell death.
- To understand the mechanism of gp120-induced neuronal apoptosis.
- To explore potential therapeutic targets for HIV-associated dementia.
Main Methods:
- In vivo studies involving intracerebroventricular injection of recombinant gp120 in rats.
- Assessment of neocortical cell death and apoptosis.
- In vitro studies of neuronal cultures exposed to gp120.
Main Results:
- Intracerebroventricular injection of recombinant gp120 induced neocortical cell death in rats.
- This cell death was confirmed to occur via apoptosis.
- Previous in vitro studies showed gp120 causes neuronal death in culture.
Conclusions:
- HIV-1 gp120 is a causative agent of neocortical neuronal apoptosis.
- This finding advances understanding of HIV-associated dementia pathophysiology.
- Identifies gp120-induced apoptosis as a potential therapeutic target.
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