Saturday April 20, 2019

New drug compound may reduce HIV potency

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Researchers have discovered that supplementing existing antiretroviral therapy with a natural compound can reduce the potency of the human immunodeficiency virus (HIV), thereby halting the progression of AIDS.

HIV-infected patients remain on antiretroviral therapy for life because the virus survives over the long-term in infected dormant cells. Interruption of current types of antiretroviral therapy results in a rebound of the virus and clinical progression to AIDS.

“OHIV_Virion-enur results highlight an alternative approach to current anti-HIV strategies,” said lead researcher Susana Valente, associate professor at The Scripps Research Institute (TSRI) in the US.

In the study published in the journal mBio, the researchers have detailed that unlike other antiretroviral therapies, a natural compound called Cortistatin A reduces residual levels of virus from the HIV-infected dormant cells, establishing a near-permanent state of latency and greatly diminishing the virus’ capacity for reactivation.

“Prior treatment with Cortistatin A significantly inhibits and delays viral rebound in the absence of any drug,” Valente noted.

“Our results suggest current antiretroviral regimens could be supplemented with a Tat inhibitor such as Cortistatin A to achieve a functional HIV-1 cure, reducing levels of the virus and preventing reactivation from latent reservoirs,” Valente explained.

For the study, the researchers isolated cells from nine HIV-infected participants being treated with antiretroviral drugs.

They found that treatment with the natural molecule reduced viral reactivation by an average of 92.3 percent. (IANS)

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Parkinson Treatment Possible Through A Blood Pressure Drug

Felodipine was effective at reducing the build-up of "aggregates" in mice with the Huntington's and Parkinson's disease mutations and in the zebrafish dementia model. 

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"This is the first time that we're aware of that a study has shown that an approved drug can slow the build-up of harmful proteins in the brains of mice using doses aiming to mimic the concentrations of the drug seen in humans," said Professor Rubinsztein. Pixabay

Felodipine, a prescribed drug to treat high blood pressure, has shown promise against Parkinson’s, Huntington’s and forms of dementia in studies carried out in mice and zebrafish at the University of Cambridge.

In a study published in the journal Nature Communications, scientists have shown in mice that felodipine may be a candidate for re-purposing.

A common feature of neurodegenerative diseases is the build-up of misfolded proteins.

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The hypertension drug was able to slow down progression of these potentially devastating conditions and “so we believe it should be trialled in patients,” he added. VOA

These proteins, such as huntingtin in Huntington’s disease and tau in some dementias, form “aggregates” that can cause irreversible damage to nerve cells in the brain.

A team led by Professor David Rubinsztein used mice that had been genetically modified to express mutations that cause Huntington’s disease or a form of Parkinson’s disease, and zebrafish that model a form of dementia.

Felodipine was effective at reducing the build-up of “aggregates” in mice with the Huntington’s and Parkinson’s disease mutations and in the zebrafish dementia model.

The treated animals also showed fewer signs of the diseases.

“This is the first time that we’re aware of that a study has shown that an approved drug can slow the build-up of harmful proteins in the brains of mice using doses aiming to mimic the concentrations of the drug seen in humans,” said Professor Rubinsztein.

The hypertension drug was able to slow down progression of these potentially devastating conditions and “so we believe it should be trialled in patients,” he added.

brain

These proteins, such as huntingtin in Huntington’s disease and tau in some dementias, form “aggregates” that can cause irreversible damage to nerve cells in the brain.
Pixabay

In healthy individuals, the body uses a mechanism to prevent the build-up of such toxic materials.

Also Read: Facebook Reveals Millions of Instagram Passwords Stored on Servers

This mechanism is known as autophagy, or ‘self-eating’, and involves cells eating and breaking down the materials.

“This is only the first stage, though. The drug will need to be tested in patients to see if it has the same effects in humans as it does in mice. We need to be cautious, but I would like to say we can be cautiously optimistic,” said Professor Rubinsztein. (IANS)