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Alzheimers Dement. 2017 Jun;13(6):644-653. doi: 10.1016/j.jalz.2016.11.005. Epub 2016 Dec 23.

Synergistic interaction between amyloid and tau predicts the progression to dementia.

Author information

1
Translational Neuroimaging Laboratory, The McGill University Research Centre for Studies in Aging, Montreal, Canada.
2
Translational Neuroimaging Laboratory, The McGill University Research Centre for Studies in Aging, Montreal, Canada; CAPES Foundation, Ministry of Education of Brazil, Brasília, Brazil.
3
Montreal Neurological Institute, Montreal, Canada.
4
Douglas Hospital Research Centre, McGill University, Montreal, Canada; Department of Epidemiology, Biostatistics & Occupational Health, McGill University, Montreal, Canada.
5
AD Research Unit, The McGill University Research Centre for Studies in Aging, Montreal, Canada; McGill University, Montreal, Canada.
6
Translational Neuroimaging Laboratory, The McGill University Research Centre for Studies in Aging, Montreal, Canada; Montreal Neurological Institute, Montreal, Canada; AD Research Unit, The McGill University Research Centre for Studies in Aging, Montreal, Canada; McGill University, Montreal, Canada; Department of Neurology and Neurosurgery, McGill University, Montreal, Canada. Electronic address: pedro.rosa@mcgill.ca.

Abstract

INTRODUCTION:

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 [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.

RESULTS:

We 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.

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.

KEYWORDS:

Alzheimer disease; Amyloid-PET; Mild cognitive impairment; Neuropsychological tests; Phosphorylated tau

PMID:
28024995
DOI:
10.1016/j.jalz.2016.11.005
[Indexed for MEDLINE]
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