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.
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.
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Results have been mixed in these trials, but Yan said the drugs might have been started too late in the disease process to help Alzheimer's patients.
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. 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.
Lead author Riqiang Yan admitted he was "shocked" when their attempts to reduce amyloid plaque in mice completely eradicated the risky build-ups that slowly cripple the brain. So the team engineered a mouse model that gradually lost the enzyme as it grew older and then bred those mice with rodents that were engineered to develop amyloid plaques from an age of 75 days.
As BACE1 plays a role in beta-amyloid production, several companies are trying to develop drugs that block the enzyme.
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These mice developed normally and appeared to remain perfectly healthy over time.
Offspring of the original BACE1 knockout mice also showed a similar reduction in their BACE1 levels. 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. Significant improvement in gliosis and neuritic dystrophy was seen with this reversal in amyloid deposition. "Those plaques caused behavioral impairment that actually reversed and significantly improved" when the plaques dissolved.
We're still in the dark as to exactly what causes Alzheimer's disease. The study, w raises hopes that drugs targeting this enzyme will be able to successfully treat Alzheimer's disease in humans. "It makes sense it might be applicable to humans as well", Kornel said.
We all know that slogging to the gym on a regular basis has positive effects on our future well-being.
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The new study was published February 14 in the Journal of Experimental Medicine.