Isn't the article saying that measures of cognitive decline aren't useful in predicting low-level amyloid deposition in a clinically unimpaired population? I'm not sure we can conclude amyloid's casual relationship with cognitive decline within a population that has no cognitive decline, right?

Thank you so much for sharing!

I know I'm a broken record on this, but that’s why silencing APP is such an important therapeutic strategy for DS-AD. Nature has already given us the proof of concept in reverse—we just have to find out if it works in clinical trials. The case for APP-targeting therapies keeps growing. (5/5)

If extra APP accelerates Alzheimer’s, reducing APP could have the opposite effect. Two well-documented cases of people with DS who were born without the extra APP copy never developed Alzheimer’s, reinforcing the idea that targeting APP could delay or prevent DS-associated Alzheimer’s. (4/5)

This supports a gene dose effect—more APP copies mean earlier Alzheimer’s. It’s highly relevant for people with Down syndrome, who have three copies of APP in all cells, just like the daughter in this case. Nearly all adults with DS develop Alzheimer’s, typically in their early 50s. (3/5)

A mother had a rare chromosomal rearrangement, leading some of her cells to have an extra APP copy. Her daughter inherited a full APP triplication in every cell. Both developed early-onset Alzheimer’s, but at very different ages: the mother at 58, the daughter at just 34. (2/5)