A paper came out in Nature recently with the mind-numbing title: “The antibody aducanumab reduces Ab plaques in Alzheimer’s disease.” But in perusal of the Abstract a statement jumped out to me: “In a transgenic mouse model of Alzheimer’s Disease (AD) aducanumab is shown to enter the brain, bind parenchymal Ab, and reduce soluble and insoluble Ab in a dose-dependent manner. In patients with prodromal or mild Ab, one year of monthly intravenous infusions of aducanumab reduces brain Ab in a dose-and time-dependent manner. This is accompanied by a slowing of clinical decline measured by Clinical Dementia Ratings-Sum of Boxes and Mini Mental State Examination scores.” They concluded that “..these results justify further development of aducanumab for the treatment of AD.”
Now, I am not in the AD-amyloid field, but this appears very exciting. I know very well that there has been a great controversy whether amyloid-plaques and tangles have anything directly to do with the clinical development of AD, but these data show that this antibody reduces brain Ab plaques. It also provides preliminary evidence for an effect on the clinical development of AZ.
But before you run out and tell your mother about this, a larger Phase 3 clinical study with many more patients must be performed, but it already gives me a warm and fuzzy feeling.
