The key to curing Alzheimer’s could be a decade’s old asthma drug after it was used to reverse dementia in mice

Researchers have successfully reversed some of the most devastating damage to the brain caused by dementia, using a decade’s old medication for treating asthma.

The study, by scientists at Temple University, centred on rolling back the buildup of tau proteins believed to be one of the core factors to the development of dementia.

Evidence points to tau proteins playing a major part in the onset of Alzheimer’s and related diseases, with tangles of these proteins blocking connections between neurons in the brain. For their study, the scientists honed in on the relationship between tau proteins and molecules known as leukotrienes, which can cause damage to nerve cells as brain diseases develop.  

“At the onset of dementia, leukotrienes attempt to protect nerve cells, but over the long term, they cause damage,”  senior investigator Domenico Praticò said. “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.”

Notably, the research wasn’t based on a newly created medication, but on a drug called zileuton, which has been in use for 22 years and typically leveraged to treat asthma.

“We show that we can intervene after disease is established and pharmacologically rescue mice that have tau-induced memory deficits,” Praticò added.

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Experimenting on mice that had been genetically engineered to have a number of tau tangles, the researchers treated the leukotrienes with zileuton – which is already known to inhibit the formation of the molecules by blocking a specific enzyme, normally in the lungs.

After 16 weeks, the mice treated with the zileuton performed much better in maze tests than their untreated brethren. They were found to have a 90% reduction in leukotrienes, and 50% fewer tau proteins. “Inflammation was completely gone from tau mice treated with the drug,” continued Praticò. “The therapy shut down inflammatory processes in the brain, allowing the tau damage to be reversed.”

The results are encouraging, although the study has some notable limitations. Firstly, the treatment only targets tau proteins, whereas dementia is also linked to the presence of beta-amyloid plaques, caused by the amyloid precursor protein (APP). There’s also the fact these trials have only been conducted in mice, so it isn’t clear whether the same treatment would work in humans.

All the same, it’s heartening news that means combating the biochemistry beneath Alzheimer’s is being developed. It’s all the more impressive in that it makes use of an already established medication, and the researchers are confident future work will bring this treatment to humans.

“This is an old drug for a new disease,” said Praticò. “The research could soon be translated to the clinic, to human patients with Alzheimer’s disease.”

The research is published in Molecular Neurobiology.