The results, published in the journal Molecular Neurobiology, showed that mice treated with "zileuton" experienced a 90 per cent reduction in the formation of leukotrienes -- inflammatory molecules that are deregulated in Alzheimer's and related dementias.
In addition, levels of phosphorylated and insoluble tau, the form of protein that is known to directly damage synapses, were 50 per cent lower.
While untreated animals had severe synaptic deterioration, the synapses of treated tau animals were indistinguishable from those of ordinary mice without the disease.
"We show that we can intervene after the disease is established and pharmacologically rescue mice that have tau-induced memory deficits," said Domenico Pratico, Professor at the varsity.
After 16 weeks, the zileuton treated tau mice performed significantly better on maze tests, suggesting a successful reversal of memory deficiency.
"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," Pratico said.
"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 noted.