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A neurotoxic fragment of the amyloid-β (Aβ) protein, Aβ1–42, and tau protein have long been incriminated as central players in the pathology of Alzheimer disease (AD). In a widely publicized study, investigators studied spinal fluid from 102 patients with well-characterized AD, 200 patients with mild cognitive impairment (MCI; a common precursor to AD), and 114 people with no measurable cognitive impairment. All participants were approximately the same age (median, 75).
Concentrations of Aβ1–42 and tau proteins created an “AD signature” that was found in 90% of patients with AD, 72% of patients with MCI, and 36% of healthy participants. Healthy participants who exhibited the “AD signature” were much more likely than the population at large t…