Journal of Gerontological Nursing

NEWS 

Alzheimer's Clue Found in Normal Brain Protein

Abstract

Scientists may be closer to identifying the triggering events that could cause the nerve degeneration of Alzheimer's disease.

A research team announced that a common brain protein, amyloid B, may damage mature cells in the central nervous system and lead to the type of cell death associated with Alzheimer's disease. Paradoxically, the same protein has been found to promote cell growth in young brain cells.

If amyloid B can be proven to be the critical factor in causing selective nerve cell loss, the next step would be to test substances that are known to block its action. These could then be the basis of future treatments for Alzheimer's disease.

Dr Bruce A. Yanknerand colleagues at the Department of Neurology, Harvard Medical School, and Children's Hospital, Boston, studied the effects of B 1-40, a specific portion of amyloid B, in both low and high concentrations on laboratory cultures of hippocampal cells from rats. The hippocampus area of the brain, essential for learning and memory, is severely affected in people with Alzheimer's disease.

The most destructive effect of amyloid B occurred at high concentrations in older cells in cultures where the protein caused an almost complete collapse of nerve growth and cell function.

While conducting these studies, the researchers recognized a similarity between the active sequence of the amyloid B protein and neuropeptides called tachykinins. The area of greatest similarity is in the part of the protein chain where most of the biological activity occurs. When tachykinins and amyloid B were placed together in dishes of cultured hippocampal cells, the destructive effects of amyloid were reversed. This finding has led to the speculation that naturally-occurring tachykinins in the brain may have the opposite effect of amyloid B. The studies suggest that tachykinins may be toxic on young, growing brain cells, but growth-enhancing for old brain cells.

For more information, contact Claudia Feldman, National Institute on Aging, 301-496-1752.…

Scientists may be closer to identifying the triggering events that could cause the nerve degeneration of Alzheimer's disease.

A research team announced that a common brain protein, amyloid B, may damage mature cells in the central nervous system and lead to the type of cell death associated with Alzheimer's disease. Paradoxically, the same protein has been found to promote cell growth in young brain cells.

If amyloid B can be proven to be the critical factor in causing selective nerve cell loss, the next step would be to test substances that are known to block its action. These could then be the basis of future treatments for Alzheimer's disease.

Dr Bruce A. Yanknerand colleagues at the Department of Neurology, Harvard Medical School, and Children's Hospital, Boston, studied the effects of B 1-40, a specific portion of amyloid B, in both low and high concentrations on laboratory cultures of hippocampal cells from rats. The hippocampus area of the brain, essential for learning and memory, is severely affected in people with Alzheimer's disease.

The most destructive effect of amyloid B occurred at high concentrations in older cells in cultures where the protein caused an almost complete collapse of nerve growth and cell function.

While conducting these studies, the researchers recognized a similarity between the active sequence of the amyloid B protein and neuropeptides called tachykinins. The area of greatest similarity is in the part of the protein chain where most of the biological activity occurs. When tachykinins and amyloid B were placed together in dishes of cultured hippocampal cells, the destructive effects of amyloid were reversed. This finding has led to the speculation that naturally-occurring tachykinins in the brain may have the opposite effect of amyloid B. The studies suggest that tachykinins may be toxic on young, growing brain cells, but growth-enhancing for old brain cells.

For more information, contact Claudia Feldman, National Institute on Aging, 301-496-1752.

10.3928/0098-9134-19910101-14

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