Monday , April 23 2018

Drugs used for HIV treatment take a toll on the brain

HIV Protease inhibitors like ritonavir and saquinavir are a crucial part of the drug cocktail that has abridged mortality in HIV-infected persons.

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New York: Antiretroviral drugs – life-changing therapies for HIV patients – might take a toll on the patient’s brain, permitting to scientists who start that the medicines lead to absent-mindedness, confusion, and behavioral changes.

These drugs lead to Neurodegeneration which is an umbrella term for the liberal loss of arrangement or function of neurons, including the death of neurons.

Certain protease inhibitors, between the most effective HIV drugs, lead to the manufacture of the peptide beta-amyloid, often connected with Alzheimer’s disease, the study found.

Researchers from the University of Pennsylvania in the US have now identified some of the key performers in causing neuronal damage. The research recommends that certain protease inhibitors, among the most effective HIV drugs, lead to the manufacture of the peptide beta-amyloid, often linked to Alzheimer’s disease.

Notably, inhibiting that enzyme, called BACE1, protected human and rodent brain cells from harm, suggesting that targeting this pathway with a new drug could minimize the damage to neurons in patients on antiretroviral therapies.

“Protease inhibitors are very active antiviral therapies, but they do have inherent toxicities,” said Kelly Jordan-Sciutto, a professor at the University of Pennsylvania.

Protease inhibitors such as ritonavir and saquinavir are a crucial part of the drug cocktail that has reduced humanity in HIV-infected people by 50%. These protease inhibitors are usually used in Africa and other developing areas hit hard by HIV/AIDS. They work by hindering viral enzymes necessary for generating infectious particles that agree that virus to spread over the body.

Earlier research has shown that protease inhibitors can have toxic effects on the central nervous system. One study verified that they triggered the initiation of stress-response pathways, including oxidative stress and a process called the unfolded-protein response, or UPR. The study performs in the American Journal of Pathology.

 

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