Some of these topics are already being researched through a five-year national clinical trial led by the O'Donnell Brain Institute.
From then on, however, the plaques began to disappear as BACE1 activity reduced, until at 10 months old no trace of them remained at all. "Sequential deletion of beta-secretase actually can reverse existing plaques".
It has therefore been a prime target in attempts to develop Alzheimer's treatments that do more than simply limit symptoms of the disease.
A year ago a trial of a drug developed by pharceutical giant Merck was abandoned before it could be completed after disappointing results.
"We need studies like this to find out how the two are intertwined and hopefully find the right formula to help prevent Alzheimer's disease", said Dr. Rong Zhang of UT Southwestern, who oversees the clinical trial and is Director of the Cerebrovascular Laboratory in the Institute for Exercise and Environmental Medicine at Texas Health Presbyterian Hospital Dallas, where the Dallas arm of the study is being carried out.
One of the earliest events in Alzheimer's disease was an abnormal build-up of beta-amyloid peptide, which could form large, amyloid plaques in the brain and disrupted the function of neuronal synapses. "In the Alzheimer's brain, a lot of those amyloid plaques accumulate and can cause neuronal loss and damage", Yan said.
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We all love to play this wonderful sport. "In this case, in this system, it would mean Hazard, Pedro and Willian are out". It's a game that we're all looking forward to. "During the game it can happen".
However, because the enzyme controls so many processes, suppressing it runs the risk of serious unwanted side effects. In many trials, mice completely lacking BACE1 suffer severe neurodevelopmental defects.
"Future studies should develop strategies to minimise the synaptic impairments arising from significant inhibition of BACE1 to achieve maximal and optimal benefits for Alzheimer's patients", said Dr Yan.
The offspring also started forming amyloid plaques at 75 days old, even though their BACE1 levels were half that of normal mice. As the second generation of mice continued to age they, though, they continued to lose BACE1 activity.
They claim their tests on a 20-month-old mouse - equivalent to a 50-year-old human - show it could be possible to halt the disease if it is caught decades earlier than usual.
The study published on Wednesday in the Journal of Experimental Medicine, showed that an enzyme called BACE1 facilitates the formation of amyloid plaques in the brains of mice with this neurodegenerative disease.