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25 May 2001. While much Alzheimer's research has focused on mechanisms
that result in the formation of amyloid plaques, a growing body of
evidence indicates that processes that break down Aβ are just as
important, and may offer novel targets for therapy. A paper by Iwata, et
al., appearing in today's Science, presents in vivo evidence that the
Aβ-degrading peptidase neprilysin plays a role in regulating Aβ
levels. The researchers "knocked out" the neprilysin gene in mice. The
lack of the gene apparently has no determinental effects on the mice.
The researchers injected Aβ peptide into the hippocampus, then 30
minutes later measured Aβ levels in the brain tissue. In normal mice
with a working neprilysin gene, 70 percent to 80 percent of the injected Aβ
was degraded, but in mice lacking one copy of neprilysin, substantially
less was degraded, and in mice lacking both copies of the gene, the
Aβ remained undegraded. The authors speculate that an age-related
decline in neprilysin could result in accumulation of Aβ to
pathogenic levels, and that a drug that boosts neprilysin levels might
be therapeutic. They also note that the neprilysin gene lies on a
stretch of chromosome 3 that has been reported to be associated with an
elevated risk of late-onset Alzheimer's.
Reference:Iwata N, Tsubuki S, Takaki Y, Shirotani K, Lu B, Gerard NP, Gerard C, Hama E, Lee HJ, Saido TC. Related Articles, Links Metabolic regulation of brain Abeta by neprilysin. Science. 2001 May 25;292(5521):1550-2. Abstract
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I recommend this paper
View all comments by Hiroshi Mori
