Comment Re:What can be done in case of a positive test? (Score 4, Informative) 45
Currently, there are no known functional cures for AD. There exist a number of treatments (monoclonal antibodies) for which there is supporting evidence for slowing cognitive decline and delaying the progression of functional disability, but the effect size is generally modest. To be fair, some people seem to be stronger responders than others; however, these amyloid-targeting treatments also have a risk of ARIA (amyloid-related imaging abnormalities), which are associated with microvascular hemorrhages (bleeding of the small blood vessels in the brain).
A subgroup of the general population is predisposed to AD because of a genetic mutation they carry (ApoE4). Each of us carries two copies of this gene, and we know that people who have one mutant copy (heterozygous) have a modestly increased risk of developing AD, and those with two mutant copies (homozygous) have a significantly higher risk. Not only is the lifetime risk increased, the typical age at onset is decades earlier; homozygotes may begin showing MCI (mild cognitive impairment) as early as in their 40s, and we call this "early-onset AD."
So, to answer your question, you are correct: there isn't really anything someone can do to stop or reverse the condition, but with early detection and treatment, they might be able to improve their quality of life and reduce the burden on caregivers and long-term financial cost of care. How such a person copes with a diagnosis is a psychological question. Some will spiral into depression and despair. Others might plan for the future in ways they might not have done otherwise, and find focus and purpose during the time they have. And it is for this latter group that the availability of such a test might be particularly helpful.
That said, having a validated and (relatively) noninvasive biomarker for AD pathology is a huge game-changer for AD research and drug development. One of the biggest challenges for targeting AD is accurately identifying the patient population. In the past, it was not always clear whether trial participants--many of whom were elderly (i.e. 75+)--actually had AD, or some other dementia, since the gold standard was to perform an autopsy. Because of this, clinical trials often suffered from a lack of statistical power due to a proportion of participants not actually having the disease that drug was intended to treat.
Since then, we devised various imaging modalities (e.g., PET) to use in conjunction with investigator assessment to improve population quality, but the more measures we have, the better the trial data gets, and the better researchers can identify targets for drug candidates. But we are still a long way off from figuring out how to prevent and/or reverse AD. One reason is that we believe that by the time patients exhibit symptoms of cognitive impairment, it's already too late--there is already extensive damage. So if there is a biomarker that can reliably detect subclinical AD pathology, this also has positive implications for designing clinical trials that aim to prevent AD disease in susceptible people, much like a vaccine for infectious disease or cancer.
It's a big dream, like being able to prevent or cure all forms of cancer. But I would like to imagine it is possible. These diseases take such a tremendous toll--on patients, on their caregivers, on the healthcare system, on society--and I hope there will come a day when they can be prevented as easily as going to your local pharmacy and getting a shot.