Alzheimer’s Disease

February 18, 2012 by staff 

Alzheimer’s Disease, On Thursday, Feb. 9, researchers at Case Western Reserve University announced in the journal Science remarkable results regarding a new treatment for mouse models of Alzheimer’s disease. The research team, led by professor of neurosciences Gary Landreth, Ph.D., discovered that a drug approved for treating skin cancers can rapidly reverse cognitive impairments in Alzheimer’s patients while also reducing their beta amyloid, a protein implicated in the disease’s progression.

While these results cannot be immediately extended to Alzheimer’s disease in humans, they are a promising new development in the treatment of a difficult and prevalent disease among older adults.

Alzheimer’s disease is marked by severe, degenerative cognitive impairment, typically in adults over age 65. The disease currently affects an estimated 5.4 million Americans, according to the Alzheimer’s Association, a nonprofit organization that funds research endeavors addressing Alzheimer’s and provides support to family caregivers.

There is currently no treatment for the disease, and a handful of symptom-slowing drugs on the market.

The drug used in the study, bexarotene, has been approved by the U.S. Food and Drug Administration for the treatment of skin cancers. Dr. Landreth’s research had previously shown that the primary cholesterol transporter in the brain, Apolipoprotein E (ApoE) clears the beta amyloid that builds up around diseased neurons and may contribute to their death.

Because bexarotene acts on the cellular signaling systems that control ApoE production, the researchers reasoned it may improve clearance of the amyloid proteins. Inheriting a particular form of ApoE is one known risk factor for Alzheimer’s disease, another promising lead for this work on the cholesterol transporter.

Paige Cramer, a Ph.D. candidate in Dr. Landreth’s lab and the lead author on this paper, is very excited about the results. When asked how her research may be more promising than similar breakthroughs in the past, Cramer said it depends on how the treatments affect the brain. “The difference between our study and others is that we are not changing the brain’s immune response or the ability of proteins to interact with each other,” Cramer said in an exclusive interview with The Observer. “Our study enhances a normal mechanism already in place.”

One remarkable part of this research is the speed with which both physiological and cognitive changes were observed following treatment with bexarotene. Within 24 hours of a single dose of bexarotene, beta amyloid levels fell by 25 percent and remained low for nearly three days.

Chronic treatment over two weeks decreased soluble beta amyloid, thought to be worse than the insoluble plaques, by 30 percent during the treatment period. The researchers examined the effects of bexarotene on several mouse strains to explore how normal and aggressive models of the disease responded. They also tested adult and aged mice, with similarly promising results across age groups.

The physiological decrease in beta amyloid was accompanied by extremely fast reversal of cognitive impairments. Bexarotene-treated mice performed significantly better on maze-navigating tests and resumed nest-making, a complex social behavior absent in untreated mouse models of Alzheimer’s disease. Bexarotene improved nest construction after just three days of treatment, while slightly longer treatments showed improved memory performance among certain mouse strains.

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