An Alzheimer’s Disease Target Identified
U.S. scientists say the protein neprilysin can reduce plaque formation and neuron death associated with Alzheimer’s disease, but at the expense of lifespan.
Thomas Jefferson University researchers said the buildup of amyloid-beta protein plaques within the brain is a hallmark of Alzheimer’s. Normally, enzymes remove the plaques, and deficiencies in those enzymes are one potential disease cause.
The scientists said neprilysin, or NEP, a major amyloid degrader, decreases naturally with age and might be the reason the elderly are more at risk for Alzheimer’s.
While studies using mice suggest enhancing NEP production has potential, the possible adverse effects of such therapy were unknown.
The new research with transgenic fruit flies expressing human NEP found a good news-bad news scenario. On the positive side, NEP expression did reduce plaque deposits and neuron damage in the flies. On the other hand, NEP also reduced the activity of important neural proteins called CREB proteins and shortened the flies’ average lifespan.
The researchers said their finding illustrates caution is needed when considering Alzheimer’s treatments, and that it’s critical to better understand normal aging when dealing with Alzheimer’s or other age-related conditions.
The study appears online in the Journal of Biological Chemistry.