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Study Furthers Understanding Of Critical Alzheimer's Disease Gene

Date:
April 8, 1999
Source:
Nih-National Institute On Aging
Summary:
Researchers have cracked part of the code for an important gene function in familial Alzheimer's disease (FAD), an early-onset type of AD. Alzheimer's disease is the most common cause of dementia. Working with cells in culture that had been altered to overexpress the amyloid precursor protein (APP), the researchers were able to document that expression of a mutant form of the presenilin-1 (PS-1) protein caused a significant reduction in the amount of amyloid formed.

Researchers have cracked part of the code for an important gene function in familial Alzheimer's disease (FAD), an early-onset type of AD. Alzheimer's disease is the most common cause of dementia. Working with cells in culture that had been altered to overexpress the amyloid precursor protein (APP), the researchers were able to document that expression of a mutant form of the presenilin-1 (PS-1) protein caused a significant reduction in the amount of amyloid formed. This continuing study of the mechanisms of plaque formation, researchers believe, moves them ever closer to the possible development of novel drugs to intervene in the processes leading up to Alzheimer's dementia.


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The above story is based on materials provided by Nih-National Institute On Aging. Note: Materials may be edited for content and length.


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Nih-National Institute On Aging. "Study Furthers Understanding Of Critical Alzheimer's Disease Gene." ScienceDaily. ScienceDaily, 8 April 1999. <www.sciencedaily.com/releases/1999/04/990408070952.htm>.
Nih-National Institute On Aging. (1999, April 8). Study Furthers Understanding Of Critical Alzheimer's Disease Gene. ScienceDaily. Retrieved April 23, 2014 from www.sciencedaily.com/releases/1999/04/990408070952.htm
Nih-National Institute On Aging. "Study Furthers Understanding Of Critical Alzheimer's Disease Gene." ScienceDaily. www.sciencedaily.com/releases/1999/04/990408070952.htm (accessed April 23, 2014).

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