Medicine

Hopes of reversing Alzheimer's raised by enzyme study

Hopes of reversing Alzheimer's raised by enzyme study

WEDNESDAY, Feb. 14, 2018 (HealthDay News) - Sustained and increasing BACE1 inhibition can reverse amyloid deposition in a mouse model of Alzheimer's disease (AD), according to a study published online Feb. 14 in the Journal of Experimental Medicine.

It improved the rodents' cognitive function - boosting learning and memory, a team at Cleveland Clinic Lerner Research Institute, US, found.

A team of researchers from the have found that gradually depleting an enzyme called BACE1 completely reverses the formation of amyloid plaques in the brains of mice with Alzheimer's disease...

Unlike previous studies that relied on study participants to assess their own fitness, the new research objectively measured cardiorespiratory fitness with a scientific formula called maximal oxygen uptake.

APECS is a randomized, placebo-controlled, parallel-group, double-blind Phase 3 clinical trial evaluating the efficacy and safety of verubecestat in people with prodromal AD. Subjects are randomized to receive placebo, or 12 mg or 40 mg verubecestat, once-daily.

As BACE1 plays a role in beta-amyloid production, several companies are trying to develop drugs that block the enzyme. An excessive accumulation of this peptide eventually leads to the Alzheimer's-related brain pathologies known as beta-amyloid plaques.

Lead author Riqiang Yan admitted he was "shocked" when their attempts to reduce amyloid plaque in mice completely eradicated the unsafe build-ups that slowly cripple the brain. These mice developed in a normal, healthy manner. To investigate whether inhibiting BACE1 in adults might be less harmful, Riqiang Yan and colleagues generated mice that gradually lose this enzyme as they grow older. These mice should have developed Alzheimer's disease, but without BACE1, they did not.

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The subsequent offspring also started building up plaque in their brains from quite an early age.

In fact, by the time they were 10 months old, the mice had no detectable beta-amyloid plaques. "Those plaques caused behavioral impairment that actually reversed and significantly improved" when the plaques dissolved. "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".

Clinical signs of Alzheimer's have been completely reversed by scientists targeting a specific brain protein, raising hopes of an effective treatment for the disease.

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.

And even if amyloids are the right target, Isaacson explained, we'd still have a minimum of five to seven years before we would know if the same approach is helpful in humans.

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


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