| Literature DB >> 12168692 |
R Jackson1, B McNeil, C Taylor, G Holl, D Ruff, E T Gwebu.
Abstract
In neurodegeneration, such as Alzheimer's disease (AD), apoptosis results in the loss of valuable neurons. A key mechanism in apoptosis is the activation of caspase-3. Caspase-3 activity first becomes detectable early in apoptosis, continues to increase as cells undergo apoptosis, and rapidly declines in late stages of apoptosis. Its activity is an early marker of cells undergoing apoptosis. Caspase-3 catalyzes the formation of beta-amyloid peptide, a hallmark of AD. The purpose of the study was to determine whether dietary aged garlic extract (AGE), with known antioxidant properties and neuroprotection against Alzheimer's beta-amyloid cytotoxicity, inhibits the caspase-3 activity in vitro. Caspase-3 activity was assayed according to the prescribed protocol and incubated overnight at ambient temperature. We report that AGE inhibits caspase-3 in dose dependent manner. Caspase-8 was not inhibited by AGE. As a caspase-3 inhibitor, AGE may be effective in reducing apoptotic death of neurons since caspase inhibitors have been shown to inhibit neuronal cell death. We propose a scheme for the ameliorative effect of AGE on deleterious effects of beta-amyloid and possibly uncontrolled caspase-3 activity.Entities:
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Year: 2002 PMID: 12168692 DOI: 10.1080/10284150290032012
Source DB: PubMed Journal: Nutr Neurosci ISSN: 1028-415X Impact factor: 4.994