***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: BACKGROUND Similar to most chronic diseases , Alzheimer 's disease ( AD ) develops slowly from a pre clinical phase into a fully expressed clinical syndrome . We aim ed to use longitudinal data to calculate the rates of amyloid β ( Aβ ) deposition , cerebral atrophy , and cognitive decline . METHODS In this prospect i ve cohort study , healthy controls , patients with mild cognitive impairment ( MCI ) , and patients with AD were assessed at enrolment and every 18 months . At every visit , participants underwent neuropsychological examination , MRI , and a carbon-11-labelled Pittsburgh compound B ( (11)C-PiB ) PET scan . We included participants with three or more (11)C-PiB PET follow-up assessment s.  Aβ burden was expressed as (11)C-PiB st and ardised uptake value ratio ( SUVR ) with the cerebellar cortex as reference region . An SUVR of 1·5 was used to discriminate high from low Aβ burdens . The slope of the regression plots over 3 - 5 years was used to estimate rates of change for Aβ deposition , MRI volumetrics , and cognition . We included those participants with a positive rate of Aβ deposition to calculate the trajectory of each variable over time . FINDINGS 200 participants ( 145 healthy controls , 36 participants with MCI , and 19 participants with AD ) were assessed at enrolment and every 18 months for a mean follow-up of 3·8 ( 95 % CI CI 3·6 - 3·9 ) years . At baseline , significantly higher Aβ burdens were noted in patients with AD ( 2·27 , SD 0·43 ) and those with MCI ( 1·94 , 0·64 ) than in healthy controls ( 1·38 , 0·39 ) . At follow-up , 163 ( 82 % ) of the 200 participants showed positive rates of Aβ accumulation . Aβ deposition was estimated to take 19·2 ( 95 % CI 16·8 - 22·5 ) years in an almost linear fashion-with a mean increase of 0·043 ( 95 % CI 0·037 - 0·049 ) SUVR per year-to go from the threshold of (11)C-PiB positivity ( 1·5 SUVR ) to the levels observed in AD . It was estimated to take 12·0 ( 95 % CI 10·1 - 14·9 ) years from the levels observed in healthy controls with low Aβ deposition ( 1·2 [ SD 0·1 ] SUVR ) to the threshold of (11)C-PiB positivity . As AD progressed , the rate of Aβ deposition slowed towards a plateau . Our projections suggest a prolonged pre clinical phase of AD in which Aβ deposition reaches our threshold of positivity at 17·0 ( 95 % CI 14·9 - 19·9 ) years , hippocampal atrophy at 4·2 ( 3·6 - 5·1 ) years , and memory impairment at 3·3 ( 2·5 - 4·5 ) years before the onset of dementia ( clinical dementia rating score 1 ) . INTERPRETATION Aβ deposition is slow and protracted , likely to extend for more than two decades . Such predictions of the rate of pre clinical changes and the onset of the clinical phase of AD will facilitate the design and timing of therapeutic interventions aim ed at modifying the course of this illness . FUNDING Science and Industry Endowment Fund ( Australia ) , The Commonwealth Scientific and Industrial Research Organisation ( Australia ) , The National Health and Medical Research Council of Australia Program and Project Grants , the Austin Hospital Medical Research Foundation , Victorian State Government , The Alzheimer 's Drug Discovery Foundation , and the Alzheimer 's Association 
    Output:
    
Conclusion Patients with aMCI showed a similar distribution of amyloid deposition determined by both visual reading and SUVR to that observed in patients with and without dementia coming to autopsy .
Most of the aMCI patients , who are already within the AD continuum , had widespread amyloid deposition in terms of amount and topographical progression .