Did the World Just Gain Hundreds of Millions of Alzheimer’s Patients?

Alzheimer’s diagnosis is shifting from a condition defined by worsening memory and independence to one that can be identified through biological markers, especially amyloid in the brain. Blood tests can now detect amyloid with accuracy approaching PET scans and spinal taps, while antibody drugs such as lecanemab and donanemab target it. This has fueled hopes that treatment could begin before symptoms appear. But the change raises a consequential question: if someone has amyloid deposits yet remains cognitively well, do they have Alzheimer’s? Donald Kewman, a healthy 76-year-old with elevated genetic risk and moderate amyloid accumulation, illustrates the uncertainty: he sees a connection to the disease, while his wife does not.

The definition has changed before. For much of the twentieth century, “Alzheimer’s disease” referred mainly to severe dementia in younger people; in the 1970s, neurologist Robert Katzman argued that it should also include late-onset dementia because both could feature plaques and tangles. That expansion brought a once-rare diagnosis to encompass most dementia in old age, despite no demonstrated single cause linking the conditions. Today’s proposed biomarker-based definition could extend the label to vast numbers of people without symptoms. The piece weighs this prospect against the limited evidence for treatment: although the new antibodies have been celebrated as a breakthrough, a large meta-study found they probably make little to no difference to memory or cognitive decline. The stakes include not only medical decisions and drug exposure, but how people understand risk, illness, and their futures.