Cerebrospinal fluid analysis detects cerebral amyloid-β accumulation earlier than positron emission tomography

作者：Sebastian Palmqvist, Niklas Mattsson, Oskar Hansson, for the Alzheimer’s Disease Neuroimaging Initiative · 发表于：Brain · 年份：2016 · DOI：10.1093/brain/aww015 · 被引用次数：404 · 研究领域：Dementia and Cognitive Impairment Research、Alzheimer's disease research and treatments、Functional Brain Connectivity Studies

See Rabinovici (doi: 10.1093/brain/aww025 ) for a scientific commentary on this article. Cerebral accumulation of amyloid-β is thought to be the starting mechanism in Alzheimer’s disease. Amyloid-β can be detected by analysis of cerebrospinal fluid amyloid-β 42 or amyloid positron emission tomography, but it is unknown if any of the methods can identify an abnormal amyloid accumulation prior to the other. Our aim was to determine whether cerebrospinal fluid amyloid-β 42 change before amyloid PET during preclinical stages of Alzheimer’s disease. We included 437 non-demented subjects from the prospective, longitudinal Alzheimer’s Disease Neuroimaging Initiative (ADNI) study. All underwent 18 F-florbetapir positron emission tomography and cerebrospinal fluid amyloid-β 42 analysis at baseline and at least one additional positron emission tomography after a mean follow-up of 2.1 years (range 1.1–4.4 years). Group classifications were based on normal and abnormal cerebrospinal fluid and positron emission tomography results at baseline. We found that cases with isolated abnormal cerebrospinal fluid amyloid-β and normal positron emission tomography at baseline accumulated amyloid with a mean rate of 1.2%/year, which was similar to the rate in cases with both abnormal cerebrospinal fluid and positron emission tomography (1.2%/year, P = 0.86). The mean accumulation rate of those with isolated abnormal cerebrospinal fluid was more than three times that of those with both normal cerebros...