July 25, 2005
July 25, 2005
Research in mice suggests that some recovery of mental function may be possible early in the course of Alzheimer’s disease. Although potential new treatments in people are likely years away, the findings may open new fronts to stop the downward spiral of memory loss and personality changes that devastate those with the illness.
Scientists worked with specially bred mice afflicted with a brain ailment similar to Alzheimer’s disease in people. They were astonished to find that rodents showing signs of dementia rapidly regained memory functions, such as the ability to locate an underwater swimming platform, after they were protected from a toxic protein called tau.
The findings suggest that some brain cells vital for memory do not die right away in the course of Alzheimer’s. ”We’d always thought the mental impairment was due to the loss of neurons,” or brain cells, says study leader Karen Ashe, professor of neurology at the University of Minnesota. ”What we’re showing is that there are neurons which are affected but not dead.”
This is not an altogether new idea. Scientists at the Fisher Center showed, at least 20 years ago, that in the early stages of Alzheimer’s disease, connections between nerve cells were lost but nerve cells themselves survived. A number of research laboratories have more recently shown that memory and problem solving in mice bred to have an Alzheimer’s-like disease can be improved by drugs that reduce levels of another toxic protein called beta amyloid.
Together these results raise the hope that, at least in the early stages of disease, treatments may one day be developed to not just halt but actually reverse memory decline. The findings were reported in the research journal Science.
New Avenues of Treatment
Doctors who study Alzheimer’s have long observed the buildup of abnormal forms of tau and beta amyloid in the brains of those with Alzheimer’s disease. Much current research is focused on the development of drugs and other treatments that may prevent this toxic buildup and preserve the health of brain cells and memory. Today’s drugs treat only the symptoms of memory loss for a limited time in some people but do little to halt or reverse the long-term progression of disease.
The current research suggests that some brain cells affected by Alzheimer’s may be “sick” and capable of being restored to health rather than becoming permanently lost. New avenues of research may lead to drugs or other therapies that prevent the buildup of tau, beta amyloid, or other toxins in the brains of those with the disease.
It’s important to note that the research was conducted in mice, and it’s a long way from rodents to humans. Still, the findings illustrate the importance of basic scientific research that helps to unravel the underlying causes of Alzheimer’s and may one day lead to effective new treatments in people.
Supporting organizations like the Fisher Center for Alzheimer’s Research Foundation is critical for funding studies that may one day lead to effective new treatments for the disease. For more information on Alzheimer’s disease treatments, or to make a donation to further research initiatives, visit www.ALZinfo.org.
SantaCruz, et al: “Tau Suppression in a Neurodegenerative Mouse Model Improves Memory Function,” Science 2005: 309, pages 476-481.