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Related Concept Videos

Encephalitis ll: Pathophysiology01:26

Encephalitis ll: Pathophysiology

Encephalitis is inflammation of the brain parenchyma caused by direct viral invasion or immune-mediated mechanisms triggered by infections or tumors. Both processes lead to neuronal injury, disrupted neurotransmission, and diverse neurological symptoms, often with overlapping clinical and pathological features.Autoimmune EncephalitisIn autoimmune encephalitis, antibodies target neuronal antigens on cell surfaces, synapses, or within neurons. A key example is anti-NMDAR encephalitis, which can...
Hepatic Encephalopathy01:29

Hepatic Encephalopathy

DefinitionHepatic encephalopathy is a reversible neurologic syndrome that results from advanced liver dysfunction or portosystemic shunting. It leads to disturbances in cognition, behavior, and motor function due to the brain’s exposure to gut-derived toxins that the liver fails to detoxify.EtiologyThis condition develops either in the setting of acute fulminant hepatitis or progressively during chronic liver disease, such as cirrhosis and portal hypertension. Portosystemic shunting—including...
Encephalitis l: Introduction01:19

Encephalitis l: Introduction

Encephalitis is inflammation of the brain parenchyma, most often due to infections or autoimmune processes. It presents with neuropsychiatric features such as fever, altered mental status, behavioral changes, cognitive dysfunction, seizures, focal deficits, and sometimes autonomic instability. In some cases, the meninges are also involved, resulting in meningoencephalitis.Infectious CausesInfectious encephalitis is most commonly viral but can also result from bacterial, fungal, or parasitic...
Alzheimer Disease ll: Pathophysiology01:23

Alzheimer Disease ll: Pathophysiology

Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and microglia. Abnormal...
Cryptococcal Meningitis01:27

Cryptococcal Meningitis

Cryptococcal meningitis is a life-threatening opportunistic infection predominantly associated with HIV/AIDS, accounting for over 100,000 deaths annually worldwide. However, it also affects individuals with other forms of immunosuppression, including those undergoing immunosuppressive therapy, organ transplant recipients, patients with innate immunodeficiencies, and individuals with hematological disorders. The infection is caused mainly by Cryptococcus neoformans and Cryptococcus gattii,...
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Dementia l: Introduction

Dementia is an acquired, progressive syndrome characterized by a decline in multiple cognitive domains severe enough to impair daily functioning and reduce independence. Although memory loss is a central feature, the diagnosis requires additional deficits involving language, executive function, visuospatial skills, judgment, calculation, or abstract reasoning. These cognitive impairments reflect underlying neurodegenerative or vascular processes that gradually disrupt neuronal networks...

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Related Experiment Video

Updated: May 28, 2026

A Rat Model of EcoHIV Brain Infection
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Published on: January 21, 2021

From Envelope to Encephalopathy: How HIV-1 gp120 Drives Neurocognitive Decline.

Maryline Santerre1, Jenny Shrestha1, Charles N S Allen1

  • 1FELS Cancer Institute for Personalized Medicine, Lewis Katz School of Medicine, Temple University, 3307 North Broad Street, Philadelphia, PA 19140, USA.

Viruses
|May 27, 2026
PubMed
Summary

HIV-1

Keywords:
BDNFCREBHIV-1 gp120NMDA receptorcalcium signalingextracellular vesiclesmitochondrial dysfunctionneuroprotectionneurotoxicityoxidative stresssenescence

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Imaging of HIV-1 Envelope-induced Virological Synapse and Signaling on Synthetic Lipid Bilayers

Published on: March 8, 2012

Area of Science:

  • Neuroscience
  • Virology
  • Immunology

Background:

  • Neurons are not productively infected by HIV-1.
  • HIV-1 envelope glycoprotein gp120 enters neurons and causes dysfunction.
  • gp120 contributes to neurobiological dysfunction in the central nervous system.

Purpose of the Study:

  • To elucidate the mechanisms by which HIV-1 gp120 causes neurobiological dysfunction.
  • To identify convergent therapeutic targets for HAND.
  • To define HAND as a network disorder.

Main Methods:

  • Investigated gp120 internalization via endocytosis and axonal transport.
  • Analyzed gp120-associated neuronal dysfunction pathways.
  • Examined the role of extracellular vesicles, microRNAs, and gut metabolites.

Main Results:

  • gp120 enters neurons through lipid raft-mediated endocytosis, macropinocytosis, and axonal transport.
  • gp120 triggers excitotoxicity, mitochondrial failure, and inflammation, suppressing CREB and BDNF signaling.
  • Extracellular vesicles, microRNAs, and quinolinic acid exacerbate gp120 effects.

Conclusions:

  • HIV-1 gp120 causes persistent neurocognitive dysfunction in HAND, independent of viral replication.
  • HAND is a network disorder involving multiple convergent pathways.
  • Combination therapies targeting excitotoxicity, mitochondrial dysfunction, and neuroinflammation are promising for neuroprotection.