Synergistic interaction between amyloid and tau predicts the progression to dementia

Male Epidemiology Apolipoprotein E4 Clinical Neurology tau Proteins Neuropsychological Tests Cellular and Molecular Neuroscience 03 medical and health sciences 0302 clinical medicine Developmental Neuroscience Alzheimer Disease Humans Cognitive Dysfunction Aged Amyloid beta-Peptides Aniline Compounds Health Policy Brain 3. Good health Psychiatry and Mental health Logistic Models Positron-Emission Tomography Disease Progression Ethylene Glycols Female Geriatrics and Gerontology Radiopharmaceuticals Biomarkers Follow-Up Studies
DOI: 10.1016/j.jalz.2016.11.005 Publication Date: 2016-12-24T08:15:27Z
ABSTRACT
AbstractIntroductionRecent literature proposes that amyloid β (Aβ) and phosphorylated tau (p‐tau) synergism accelerates biomarker abnormalities in controls. Yet, it remains to be answered whether this synergism is the driving force behind Alzheimer disease (AD) dementia.MethodsWe stratified 314 mild cognitive impairment individuals using [18F]florbetapir positron emission tomography Aβ imaging and cerebrospinal fluid p‐tau. Regression and voxel‐based logistic regression models with interaction terms evaluated 2‐year changes in cognition and clinical status as a function of baseline biomarkers.ResultsWe found that the synergism between [18F]florbetapir and p‐tau, rather than their additive effects, was associated with the cognitive decline and progression to AD. Furthermore, voxel‐based analysis revealed that temporal and inferior parietal were the regions where the synergism determined an increased likelihood of developing AD.DiscussionTogether, the present results support that progression to AD dementia is driven by the synergistic rather than a mere additive effect between Aβ and p‐tau proteins.
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