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Synergistic interaction between amyloid and tau predicts the progression to dementia
Author(s) -
Pascoal Tharick A.,
Mathotaarachchi Sulantha,
Shin Monica,
Benedet Andrea L.,
Mohades Sara,
Wang Seqian,
Beaudry Tom,
Kang Min Su,
Soucy JeanPaul,
Labbe Aurelie,
Gauthier Serge,
RosaNeto Pedro
Publication year - 2017
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2016.11.005
Subject(s) - dementia , voxel , positron emission tomography , biomarker , logistic regression , oncology , cognition , psychology , medicine , cognitive decline , tau protein , disease , amyloid (mycology) , neuroscience , alzheimer's disease , pathology , chemistry , radiology , biochemistry
Recent 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. Methods We stratified 314 mild cognitive impairment individuals using [ 18 F]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. Results We found that the synergism between [ 18 F]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. Discussion Together, 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.