Researchers successfully reverse Alzheimer's in mice giving hope to human trials

Researchers successfully reverse Alzheimer's in mice giving hope to human trials

And the rodents' intellectual function actually improved as their amyloid plaques dissolved from lack of beta-secretase (BACE1), an enzyme critical in the formation of the plaques, said senior researcher Riqiang Yan.

The researchers found that amyloid deposition was completely reversed with sequential and increased deletion of BACE1 in an adult AD mouse model.

Scientists at the Cleveland Clinic theorized that reducing BACE1 in the brain would have a trickle down effect, reducing plaque formation.

But the once-exciting trial has slowly spluttered to a halt: the firm shelved a similar trial of the same drug Verubecestat in late-stage patients past year, but had hoped it could work in early or mid-stage sufferers. The results further bolster the theory that amyloid plaques are at the root of this mysterious brain disease, and that addressing these plaques could lead to an eventual cure for Alzheimer's.

Amyloid plaques are believed to contribute to Alzheimer's disease because the sticky clumps could interfere with communications between brain synapses.

As BACE1 plays a role in beta-amyloid production, several companies are trying to develop drugs that block the enzyme.

Dr Riqiang Yan, of the Cleveland Clinic Lerner Research Institute in the USA, said: "To our knowledge, this is the first observation of such a dramatic reversal of amyloid deposition in any study of Alzheimer's disease mouse models". Instead they developed normally and remained healthy well into old age.

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The offspring also started forming amyloid plaques at 75 days old, even though their BACE1 levels were half that of normal mice. Remarkably, however, the plaques began to disappear as the mice continued to age and lose BACE1 activity, until, at 10 months old, the mice had no plaques in their brains at all.

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"The completely other side of the coin is that 99 percent of all clinical drug trials [for Alzheimer's disease] have failed and we don't know why", said Isaacson, who was not involved in the new study. "We are grateful to the patients and caregivers who participated in this study, and despite this outcome, Merck remains committed to developing novel therapies for the treatment of Alzheimer's and other neurodegenerative diseases".

Still, Dr. Daniel Franc, a neurologist at Providence Saint John's Health Center in Santa Monica, California, said that regardless of whether this exact finding can be successfully translated to humans, the results are still important.

Yan envisions a future when these enzymes, known as BACE1 inhibitors, could be available as a vitamin that all humans take preventatively to stave off neurodegenerative disease.

The study published in the Journal of Alzheimer's Disease focused on a type of brain tissue called white matter, which is composed of millions of bundles of nerve fibres used by neurons to communicate across the brain.

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