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Alzheimer's Disease

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Approximately 4 million Americans currently have Alzheimer's; an estimated 14 million will have the disease by the middle of this century (2050) unless a cure or prevention is found.
One in 10 persons over 65 and nearly half of those over 85 have Alzheimer's disease.
The average lifetime cost per patient is $174,000, and total disease-associated costs reach $100 billion a year in the United States. Former generations may have refered to an elderly family member's odd manner as preoccupied or eccentric. Now, however, signs of erratic behavior or memory lapses trigger concerns about what has come to be recognized as the medical condition Alzheimer's disease.

The underlying causes of Alzheimer's are unclear, but the results—ravaged and dead nerve cells in the brain, accompanied by memory loss—suggest that the most effective ways to battle the disease may be to help brain cells survive or, if possible, replace cells lost to the disease. Sanford-Burnham scientists are working toward these goals on several fronts.

Your Health

Sanford-Burnham research on Alzheimer's disease

Professor Stuart Lipton and his team in the Del E. Webb Center for Neuroscience, Aging, and Stem Cell Research are examining the role of molecular gates called ion channels, in both normal brain function and disease states. These pores in the membranes surrounding nerve cells regulate transit of ions—charged forms of calcium, sodium and potassium—in and out of nerve cells. A balanced flow is essential to normal learning and memory formation, but a flood of ions can be harmful, even lethal, to brain cells.

Lipton's laboratory recently showed that a drug called Memantine can help protect brain cells against excess ion flow by partially blocking channels. Because ion flow is critical to normal brain activity, complete blockage causes severe side effects such as hallucinations or seizures. Memantine has been shown to slow progression of Alzheimer's and was approved in 2002 for this purpose in Europe; FDA approval is pending.

More than one path to brain cell death

Mutations in a family of genes called presenilins are the most common cause of familial Alzheimer's and have been implicated in the formation of plaques that riddle the brains of patients with the disease. Associate Professor Zhuohua Zhang and his colleagues have intriguing evidence that partially inhibiting one member of the presenilin family can help brain cells survive.