Alzheimer’s disease develops slowly from a preclinical phase into a fully expressed clinical syndrome. The present study used longitudinal data to calculate the rates of amyloid-beta (Aβ) deposition, cerebral atrophy, and cognitive decline.

In this prospective cohort study, 145 healthy controls, 36 patients with mild cognitive impairment (MCI), and 19 patients with Alzheimer’s disease were assessed at enrolment and every 18 months for a mean follow-up of 3.8 years. At baseline, significantly higher amyloid-beta levels were noted in patients with Alzheimer’s and those with MCI compared to healthy controls.

At follow-up, 82% of the 200 participants showed positive rates of amyloid-beta accumulation. Amyloid-beta deposition was estimated to take 19·2 years in an almost linear fashion to go from the threshold of 11C-PiB positivity to the levels observed in Alzheimer’s disease.

It was estimated to take 12·0 years from the levels observed in healthy controls with low amyloid-beta deposition to the threshold of 11C-PiB positivity. As Alzheimer’s progressed, the rate of amyloid-beta deposition slowed towards a plateau. Our projections suggest a prolonged preclinical phase of Alzheimer’s disease in which amyloid-beta deposition reaches our threshold of positivity at 17·0 years, hippocampal atrophy at 4·2 years, and memory impairment at 3·3 years before the onset of dementia.

Understanding the time course of this disorder should facilitate the timing of therapeutic interventions aimed at modifying the course of this illness.

 Villemagne VL, Burnham S, Bourgeat P, Brown B, Ellis KA, Salvado O, Szoeke C, Macaulay SL, Martins R, Maruff P, Ames D, Rowe CC, Masters CL, for the Australian Imaging Biomarkers and Lifestyle (AIBL) Research Group: Amyloid β deposition, neurodegeneration, and cognitive decline in sporadic Alzheimer’s disease: a prospective cohort study. Lancet Neurology 12(4): 357-367 (2013).

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