Every two weeks, a nurse visits 43-year-old Marty Reiswig in Denver, Colorado, and injects him with an experimental drug called gantenerumab.
Every month, Reiswig drives into town for a brain scan to make sure the drug has not caused any bleeds.
And every year he flies to St Louis, Missouri, for four days of brain scans, spinal taps, blood analyses and exhaustive tests of his memory and reasoning capacity.
Reiswig is fit and healthy and runs two local businesses. He goes through all of this because he has a rare genetic mutation that almost guarantees he will develop early-onset Alzheimer’s disease.
He hopes that the international clinical trial he has been part of for nine years might prevent, or at least delay, the onset of symptoms that will otherwise arise in just a few years’ time.
The trial is one of several trying to understand whether treating the root cause of Alzheimer’s before symptoms start might be the best way to handle a disease that exacts such a large toll.
The drugs under scrutiny are all antibodies that have been developed to target and clear amyloid-β proteins in the brain, which clog together into toxic masses called plaques (see ‘Antibodies against amyloid’).