The protein named amyloid-β (Aβ) is the main component of the amyloid plaques and part of a cascade of reactions that, along with neurofibrillary tangles, are found in the brains of those afflicted with Alzheimer’s Disease (AD). They are thought to be causative. Several anti-Aβ therapies are under development and a few are already being clinically tested. Unfortunately, thus far no attempts to attack Aβ therapeutically have succeeded.
That is until now. There was exciting news this week: In an article by Sevigny et. al. in the scientific journal Nature, it was reported that a human monoclonal antibody called aducanumab has been found to reduce the amyloid plaques in patients with AD. They had been diagnosed with the affliction by means of positron emission tomography (PET) scans and standard dementia testing. Of most importance, the diminished Aβ determination in these patients coincided with the finding that there was a parallel improvement in their mental decline using the same dementia test. The journal stated that “confirmation of a cognitive benefit would be a game-changer.”
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