Memory deficits linked to Alzheimer’s disease were reversed in mice treated with an anti-cancer drug, according to researchers at the University of Pittsburgh Graduate School of Public Health.

The study’s authors were studying mice expressing human Apolipoprotein E4 (APOE4), the only firmly established genetic risk factor for late-onset Alzheimer’s disease, or APOE3, which is known not to increase the risk for Alzheimer’s disease, when another study was published stating that the drug bexarotene improved memory and rapidly cleared amyloid plaques from the brains of Alzheimer’s model mice expressing mouse Apolipoprotein E (APOE).

Amyloid plaques consist of toxic protein fragments called amyloid beta that appear to damage neurons in the brain and are believed to cause the associated memory deficits of Alzheimer’s disease and, ultimately, death.

Moreover, Bexarotene is a compound chemically related to vitamin A that activates Retinoic X Receptors (RXR) found everywhere in the body. Once activated, the receptors bind to DNA and regulate the expression of genes that control a variety of biological processes. Among its effects is increased levels of APOE.

“We were already set up to repeat the [other] study to see if we could independently arrive at the same findings,” co-author Dr. Iliya Lefterov, associate professor in Pitt Public Health’s Department of Environmental and Occupational Health, said in a statement.

And while the team was able to verify that the mice quickly regained their lost cognitive abilities as well as demonstrate a decrease in amyloid beta peptides in the interstitial fluid that surrounds brain cells, they were not able to find any evidence that the drug cleared the plaques from their brains, according to Lefterov.

The scientists hypothesize that the drug works through a number of different biological process, perhaps by reducing soluble oligomers which, like the plaques, are composed of the toxic amyloid beta protein fragments.

However, the oligomers are composed of smaller amounts of amyloid beta and, unlike the plaques, are still able to “move.”

“We did find a significant decrease in soluble oligomers,” said senior author Dr. Rada Koldamova, associate professor in Pitt Public Health’s Department of Environmental and Occupational Health.

For this reason the scientists believe it’s possible that the oligomers are more dangerous than the plaques in people with Alzheimer’s disease and that it may be possible that the improvement of cognitive skills in mice treated with bexarotene is not related to amyloid beta but for a reason that remains unknown as of yet.

Based on their findings, the scientists believe more research should be conducted in relation to bexarotene as a therapeutic treatment for Alzheimer’s disease..

This work was supported by grants from the National Institute of Health and the Alzheimer’s Association.