Researchers Observe Dementia Reversal In Mice

Dementia patients have renewed hope of being cured of their ailment following a successful study in which researchers managed to reverse dementia in mice.

 

The study, which was conducted recently, represents the very first time that tau pathology reversal was documented in an animal model.

Tauopathy is a term used to refer to a specific type of neurodegenerative disease, which results in the second-most significant lesion that develops in Alzheimer’s sufferers’ brains. Tauopathy presents itself when proteins get tangled after dissociating from microtubules and form aggregates of protein on the brain that are insoluble.

"We show that we can intervene after the disease is established and pharmacologically rescue mice that have tau-induced memory deficits," said senior researcher. 

 

The breakthrough came through the observation of leukotrienes, which are inflammatory molecules that play a significant role in dementia, with particular reference to its latter stages of development.
"At the onset of dementia, leukotrienes attempt to protect nerve cells, but over the long term, they cause damage," the researcher explained. "Having discovered this, we wanted to know whether blocking leukotrienes could reverse the damage, whether we could do something to fix memory and learning impairments in mice having already abundant tau pathology."
It must be said that testing this particular hypothesis was no mean feat – the team used mice that were specifically engineered with the tau pathology as they aged. The researchers waited until the animals were 12 months old, or 60 years old in human years before they treated them with zileuton, a leukotriene inhibitor.

 

The mice used in the study were administered zileuton treatment over the course of 16 weeks, then put through a variety of mazes to test their memory. Zileuton-treated mice were seen to fare much better than those that were administered none. As a result, researchers believe that zileuton treatment can actually reverse memory deficiencies in mice.

Further analysis determined that mice treated with zileuton experienced a 90% reduction in leukotrienes compared to the mice that were administered none. What’s more is that the treated mice had a 50% lower concentration of insoluble tau – known to damage brain synapses – than their untreated counterparts.
"The inflammation was completely gone from tau mice treated with the drug. The therapy shut down inflammatory processes in the brain, allowing the tau damage to be reversed," the researcher said.

"Leukotrienes are in the lungs and the brain, but we now know that in addition to their functional role in asthma, they also have a functional role in dementia. This is an old drug for a new disease. The research could soon be translated to the clinic, to human patients with Alzheimer's disease,” he added.

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Protein that helps HIV to evade the body's defence system discovered

Researchers have discovered the protein that helps HIV to evade the body's defense system, an advance that may help stop the deadly virus in its tracks.

When HIV-1 infects an immune cell, the virus travels to the nucleus so quickly there is not enough time to set off the cells alarm system.

Now, researchers  have discovered the protein that helps the virus travel so fast.

The researchers found that without this protein, the virus became stranded in the cytoplasm, where it was detected by the viral defense system.

"By preventing its normal movement, we essentially turned HIV-1 into a sitting duck for cellular sensors," said  an associate professor.

HIV-1 infects and kills immune system cells, including T cells and macrophages that were used in the study.

This cripples the immune system, making the patient vulnerable to common bacteria, viruses and other pathogens that are usually harmless in people with healthy immune systems.

After HIV-1 enters a cell, it has to work its way through the cytoplasm to the nucleus. Once inside the nucleus, HIV-1 takes control of the cell and makes additional HIV-1 copies.

However, getting through the cytoplasm is not easy. Cytoplasm consists of fluid that is thick with proteins and structures such as mitochondria.

"Something the size of a virus cannot just diffuse through the cytoplasm," said an author of the study published.

"It would be like trying to float to the bathroom in a very crowded bar. You need to have a plan," said the author.

HIV-1 is able to get to the nucleus quickly via tubular tracks called microtubules. The virus attaches itself to a molecular motor called dynein, which moves down the microtubule like a train car on tracks.

Researchers discovered the "ticket" HIV-1 needs to get on the train - a protein called bicaudal D2.

HIV-1 binds to bicaudal D2, which recruits the dynein molecular motor. The dynein then transports HIV-1 towards the nucleus.

The finding raises the possibility of developing a drug that would prevent HIV-1 from binding to bicaudal D2, thus stranding the virus in the cytoplasm.

This would not only prevent infection, but also give the cell time to turn on antiviral genes that would protect it and neighbouring cells from infection.

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