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

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The piece examines whether Alzheimer’s should be defined by biological changes in the brain, even before memory or thinking problems appear. New blood tests can detect amyloid, a protein associated with the disease, with accuracy approaching PET scans and spinal taps; the FDA cleared its first such test in 2025. Combined with recently approved amyloid-targeting drugs, these tests have fueled hopes that treatment could begin early enough to prevent symptoms. But they also raise a consequential question: whether people with amyloid deposits but normal cognition should be considered to have Alzheimer’s. Donald Kewman, a cognitively healthy man with genetic risk and moderate amyloid accumulation, illustrates the ambiguity: he sees a sense in which he has the disease, while his wife does not.

The debate reflects a shifting definition. Alois Alzheimer identified plaques, tau tangles, and neuron loss in the brain of a woman with severe early-onset dementia in 1906; for decades, the disease’s name chiefly described dementia in younger people. In the 1970s, neurologist Robert Katzman argued that late-onset dementia should also count as Alzheimer’s because it shared features with early-onset cases, despite lacking proof of one common cause. That expansion made a rare diagnosis encompass much of old-age dementia and helped raise its institutional profile. Today’s proposed move from symptoms to biomarkers could expand the label far further. The optimism about treatment is also contested: a large meta-study found amyloid antibodies probably make little to no difference to memory and cognitive decline.

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