Making Alzheimer's a Better Memory

Alzheimers disease in mice reversed with bexarotene

(RxWiki News) Could this dream come true? A medication that's currently approved for one disease could make Alzheimer's disease nothing more than a nightmarish memory.

If an animal study can be confirmed in humans, this dream might just come true.

A drug approved to treat skin cancer - Targretin (bexarotene) - has been shown to reverse Alzheimer's in mice by quickly clearing proteins linked to the disease. And while these are encouraging findings, more study is needed to see if the medication can be safely used with humans .

"Find out about all approved medications to treat Alzheimer's disease."

A progressive brain disorder, Alzheimer's eventually destroys an individuals memory and thinking abilities.

Gary Landreth, Ph.D., of Case Western Reserve University, and colleagues used what's currently known about Alzheimer's to search for a drug that might help treat it.

It is known that in the most common form of the disorder, the brain has too much of a sticky protein fragment known as beta-amyloid. These fragments clump together to form plaques that disrupt normal brain function.

Healthy people produce another protein called  apolipoprotein E (ApoE) which clears away the excess beta-amyloid. Some patients with Alzheimer's may not make enough of this protein, which causes an overload of beta-amyloid.

Landreth's team set about looking for a medication that could increase ApoE production when they found bexarotene, which does exactly that to treat skin cancer.

Researchers gave the medication to mice models that develop amyloid plaques to show how Alzheimer's behave.

When given to these animals, bexarotene quickly (sometimes in a matter of hours) reduced beta-amyloid levels in mice of all ages and reduced the size of plaques in most. 

The youngest mice responded the most quickly, with levels falling sharply a mere six hours after after receiving the drug. In 6-month-old mice,a 14-day regimen of daily doses of bexarotene dropped beta-amyloid levels by a sustained 30 percent drop, and plaques were reduced by about 75 percent.

The drug also reversed behavioral symptoms in the mice including memory, cognitive function (being able to figure out a maze), social behavior (nesting). The ability to smell (often the first sign of Alzheimer's)  was also resorted.

These are preliminary findings, but suggest that boosting ApoE activity may be a way of curtailing the progression of Alzheimer's disease.

Although preliminary, the results suggest that treatments aimed at boosting ApoE activity might be an effective approach for blocking the progression of Alzheimer’s disease.

“This is a particularly exciting and rewarding study because of the new science we have discovered and the potential promise of a therapy for Alzheimer's disease,” says Landreth. "Our next objective is to ascertain if it acts similarly in humans," he added.

 The results of this study appeared in the February 9, 2012, advance online edition of Science.

The research was supported in part by the National Institutes of Health National Institute on Aging (NIA) and National Institute on Deafness and Other Communication Disorders (NIDCD).