Neurology: A 10-year follow-up found that early reduction of A-beta deposition may help prevent Alzheimer's disease

The clinical manifestations of Alzheimer's disease (AD) occur decades before the incubation period, when amyloid (A beta) and tau proteins accumulate into pathological forms and are likely to play an important role.
amyloid hypothesis is a widely accepted disease pathogenesis model that assumes that A-beta is the earliest initiation event in this pathological chain.
, many treatment trials, while reducing brain A-beta in AD patients, did not produce clinically improved results, so this model was called into question.
new approach recommends "primary prevention" for anti-A-beta therapy before symptoms appear, even before brain A-beta deposition is detected.
treatment, which begins early, requires an understanding of the timing of brain A beta deposition.
most existing amyloid PET longitudinal studies are limited by the sample size and follow-up time.
The Alzheimer's Neuroimaging Program (ADNI) began collecting continuous amyloid-florbetapir (FBP) PET scans in 2010 and has been tracking some of the participants to this day.
in this study, they used up to six consecutive FBP scans and a maximum follow-up time of nine years to estimate changes in cognitive normality and impair the A-beta dynamics of individuals to predict the process of change from cognitive normality to impairment.
, William J Jagust of the University of California, Berkeley, et al., based on the well-known Alzheimer's Disease Neuroimaging Initiative, explores the relationship between the cognitive normality of A-beta-negative and the time process and cognitive prognostication of the positive conversion of A-beta-positive.
they studied two samples of ADNI participants using a sample of ADNI using s18F-Florbetapir, FBP) A-PET, and followed them for up to 9 years.
sample A included 475 cognitively normal (CN) seniors and patients with mild cognitive impairment (MCI) and AD, and sample B included 220 CN A beta-individuals.
, the trajectory of FBP in sample A over time, and the rate at which A-beta PET scans in sample B changed from negative to positive.
results show.
between the time of the test and brain A beta is S-shaped, and it takes 6.4 years to change from amyloid-negative to positive, and 13.9 years to mcCI.
A beta deposition rate began to slow down 3.8 years after the positive threshold was reached.
the risk of A-beta-positive was 38/1000 years, and the factors associated with conversion (from negative to positive) were age, baseline FBP, and female carriers of lipoprotein E4.
in CN A beta-individuals, FBP slope was associated with memory decline and brain tau measured five years after the baseline with the Flortaucipir PET.
important for this study is the discovery that reducing brain A beta should be done early in AD evolution.
transition from A-beta-to-A-beta-plus for PET scans should be predictable, so reducing the progression of beta-A at an early stage may yield significant clinical benefits.
original origin: Jagust, W. J., Landau, S.M., and Alzheimer's Disease Neuroimaging Initiative. Temporal Dynamics of Beta-amyloid Accumulation in Aging and Alzheimer’s Disease. _Neurology_. Freeman Source: MedSci Original Copyright Notice: All text, images and audio and video materials on this website that indicate "Source: Mets Medicine" or "Source: MedSci Originals" are owned by Mets Medical and are not reproduced by any media, website or individual without authorization, and are authorized to be reproduced with the words "Source: Mets Medicine".
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