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Clues found for early memory loss in Alzheimer's disease

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By Press Release by the National Institutes of Health • • April 7, 1994

Scientists at the National Institute of Neurological Disorders and Stroke (NINDS) have discovered that adding a substance called beta amyloid to normal skin cells causes the cells to exhibit the same type of molecular dysfunction previously demonstrated in skin cells of patients with Alzheimer's disease (AD). This step may lead to a new explanation of memory loss, one of the earliest and most common symptoms of the disease. The study will be published in the April 8, 1994 issue of Science.

By placing a solution of low-level beta amyloid in culture with normal human fibroblasts, or skin cells, the scientists produced changes in potassium channel function similar to changes observed in cells from AD patients. Last year, the same laboratory demonstrated that skin cells from people with AD have defects that upset the cell's ability to properly regulate potassium and calcium ions. The flow of potassium and consequent uptake of calcium are especially critical in cells responsible for memory formation and storage.
Beta amyloid is a protein that is the main component of plaques, the patches of destroyed brain tissue which, together with neurofibrillary tangles, are the classic hallmark of Alzheimer's disease.

"For many years scientists have been trying to understand the relationship between memory loss and plaques in the brain and, indeed, to determine what role beta amyloid plays in the early stages of AD. What this finding suggests is that soluble beta amyloid may cause the dysfunction that leads to memory loss even before the insoluble form congeals into plaques," said Daniel L. Alkon, M.D., chief of the NINDS Laboratory of Adaptive Systems, where the work was conducted, and an author of the paper.

"If we can understand what is happening in the cellular process early enough in the course of Alzheimer's disease, we may move closer to learning how to intervene and halt the deadly progression of this disease. This study points us in that direction," said Patricia A. Grady, Ph.D., Acting Director of NINDS.

The Science paper expands upon and validates the earlier study by Dr. Alkon's laboratory that described a possible skin test for diagnosing AD based on the differences found in the skin cells of AD patients. Their work was published in the Sept. 1, 1993 Proceedings of the National Academy of Sciences.** The earlier study showed that the skin cells of people with AD were missing a certain type of microscopic tunnel (the 113pS potassium channel) that governs the flow of potassium in and out of the cells. Of 44 people tested, skin cells from the 13 who were clinically diagnosed with AD were missing the potassium channel, whereas nearly all of the people in the control group had functional potassium channels of the same type.

In the current study, researchers found that after treating one group of the cells with soluble beta amyloid for 48 hours, the 113pS potassium channel was absent in all but one of the cells. However, the functional potassium channel was present in 94% of a group of untreated cells. After conducting a variety of similar tests, the scientists concluded that beta amyloid seems to selectively target this specific potassium channel, which they had observed to be absent in skin cells of AD patients.

"The fact that low concentrations of beta amyloid can disrupt the function of this key potassium channel may be a clue to what's happening in the brain to cause early memory loss in Alzheimer's patients," said Dr. Alkon. Researchers in Dr. Alkon's laboratory are now at work on the next step--to see if similar potassium channel dysfunction occurs in central nervous system neurons. The scientists have discovered similar defects in nerve cells of the olfactory system, suggesting that such defects may also be present in brain cells.

AD is the single greatest cause of intellectual impairment in older Americans, affecting more than 2.5 million people in the United States alone. The disorder causes a progressive and irreversible dementia, or mental decline.

Source: National Institutes of Health
US Department of Health and Human Service
Press Release
April 7, 1994

Reference: *Rene Etcheberrigaray, M.D., Etsuro Ito, Ph.D., Christopher S. Kim, Daniel L. Alkon, M.D. "Soluble b-Amyloid Induction of Alzheimer's Phenotype for Human Fibroblast K+ Channels," Science, Vol. 264, April 8, 1994 (pp. 276-278).
**Rene Etcheberrigaray, Etsuro Ito, Kotaro Oka, Beth Tofel-Grehl, Gary E. Gibson and Daniel L. Alkon. "Potassium channel dysfunction in fibroblasts identifies patients with Alzheimer disease," PNAS, Sept. 1, 1993 (pp. 8209-8213).

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