Alzheimer's disease reversed in mice, offering hope for humans, new research shows

Ebony Scott
February 17, 2018

Lead writer Riqiang Yan worked with colleagues to breed mice that would gradually lose the BACE1 enzyme as they aged. That is now in phase 3 clinical trials.

In particular, the scientists successfully rollbacked the formation of unsafe amyloid plaques in the brains of mice, paving the way for similar treatments in humans.

In fact, mice that lack the enzyme completely suffer from severe deficits of neurological development.

Decreasing BACE1 activity also resulted in lower beta-amyloid peptide levels and reversed other hallmarks of Alzheimer's disease, such as the activation of microglial cells and the formation of abnormal neuronal processes. Once it was established that these animals developed healthily they were bred with other mice that had been bred to develop amyloid plaques when they hit 75 days old.

But as the mice continued to age and lose BACE1 activity, the plaques that already had formed in their brains began to disappear.

'We were surprised it worked so well, we saw complete reversal, ' Yan, who will start as chair of the department of neuroscience at the University of CT this spring, said.

For the study, researchers enrolled more than 80 older patients at high risk of developing Alzheimer's disease and had early signs of memory loss, or even mild cognitive impairment.

"They seem to think that inhibiting BACE1 will have the best impact if you go early, because you'll prevent the accumulation of amyloid plaques and, for the plaques that do form, you'll have a healthy brain that has the mechanisms in place that can clear those plaques out", Hendrix said.

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The lab study provides additional confirmation that BACE1 could play an important role in Alzheimer's disease, particularly if the enzyme is inhibited at the right time, said James Hendrix, director of global science initiatives at the Alzheimer's Association.

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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 was supported by grants from the National Institutes of Health.

"That enzyme for sure is active. It makes sense it might be applicable to humans as well", Kornel said.

'Our tests on a 20-month-old mouse found no side effects, now we have to look at a much older mouse to see if this can work in later stages of disease'.

The new study was published February 14 in the Journal of Experimental Medicine.

The new study from a team at the Cleveland Clinic Lerner Research Institute focused on an enzyme called BACE1 (aka beta-secretase), which is known to contribute to the formation of the toxic amyloid proteins that congregate as plaques on the brain, and are hypothesized to be the source of most Alzheimer's symptoms.

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