Time to Amyloid Positivity and Preclinical Changes in Brain Metabolism, Atrophy, and Cognition: Evidence for Emerging Amyloid Pathology in Alzheimer's Disease
Abstract
Background: Aβ pathology is associated with longitudinal changes of brain metabolism, atrophy, and cognition, in cognitively healthy elders. However, Aβ information is usually measured cross-sectionally and dichotomized to classify subjects as Aβ-positive or Aβ-negative, making it difficult to evaluate when brain and cognitive changes occur with respect to emerging Aβ pathology. In this study, we use longitudinal Aβ information to combine the level and rate of change of Aβ to estimate the time to Aβ-positivity for each subject and test this temporal proximity to significant Aβ pathology for associations with brain structure, metabolism, and cognition. Methods: In 89 cognitively healthy elders with up to 10 years of follow-up, we estimated the points at which rates of fluorodeoxyglucose (FDG) PET, MRI, and cognitive and functional decline begin to accelerate with respect to the time to Aβ-positivity. Points of initial acceleration in rates of decline were estimated using mixed-effects models with penalized regression splines. Results: Acceleration of rates of FDG PET were observed to occur 20+ years before the conventional threshold for Aβ-positivity. Subtle signs of cognitive dysfunction were observed 10+ years before Aβ-positivity. Conclusions: Aβ may have subtle associations with other hallmarks of Alzheimer’s disease before Aβ biomarkers reach conventional thresholdsmore »
- Authors:
-
- Lund Univ. (Sweden). Dept. of Clinical Sciences Malmo. Clinical Memory Research Unit; Center for Imaging of Neurodegenerative Diseases, San Francisco, CA (United States). Dept. of Veterans Affairs Medical Center; Univ. of California, San Francisco, CA (United States). Dept. of Radiology and Biomedical Imaging
- Vrije Univ., Amsterdam (Netherlands). Neuroscience Campus Amsterdam. Dept. of Neurology and Alzheimercenter
- Univ. of Southern California, San Diego, CA (United States). Alzheimer's Therapeutic Research Inst.
- Univ. of California, Berkeley, CA (United States). Helen Wills Neuroscience Inst.; Lawrence Berkeley National Lab. (LBNL), Berkeley, CA (United States). Life Sciences Division
- Lund Univ. (Sweden). Dept. of Clinical Sciences Malmo. Clinical Memory Research Unit; Skåne University Hospital, Malmö (Sweden). Memory Clinic
- Center for Imaging of Neurodegenerative Diseases, San Francisco, CA (United States). Dept. of Veterans Affairs Medical Center; Univ. of California, San Francisco, CA (United States). Dept. of Radiology and Biomedical Imaging
- Lund Univ. (Sweden). Dept. of Clinical Sciences Malmo. Clinical Memory Research Unit; Skåne University Hospital, Malmö (Sweden). Memory Clinic; Skåne University Hospital, Malmö (Sweden). Dept. of Neurology
- Publication Date:
- Research Org.:
- Lawrence Berkeley National Laboratory (LBNL), Berkeley, CA (United States)
- Sponsoring Org.:
- USDOE Office of Science (SC), Biological and Environmental Research (BER). Biological Systems Science Division
- OSTI Identifier:
- 1628204
- Grant/Contract Number:
- AC02-05CH11231
- Resource Type:
- Accepted Manuscript
- Journal Name:
- Frontiers in Neuroscience (Online)
- Additional Journal Information:
- Journal Name: Frontiers in Neuroscience (Online); Journal Volume: 11; Journal ID: ISSN 1662-453X
- Publisher:
- Frontiers Research Foundation
- Country of Publication:
- United States
- Language:
- English
- Subject:
- 59 BASIC BIOLOGICAL SCIENCES; Neurosciences & Neurology; Alzheimer’s disease; β-amyloid; atrophy; metabolism; cognition; preclinical
Citation Formats
Insel, Philip S., Ossenkoppele, Rik, Gessert, Devon, Jagust, William, Landau, Susan, Hansson, Oskar, Weiner, Michael W., and Mattsson, Niklas. Time to Amyloid Positivity and Preclinical Changes in Brain Metabolism, Atrophy, and Cognition: Evidence for Emerging Amyloid Pathology in Alzheimer's Disease. United States: N. p., 2017.
Web. doi:10.3389/fnins.2017.00281.
Insel, Philip S., Ossenkoppele, Rik, Gessert, Devon, Jagust, William, Landau, Susan, Hansson, Oskar, Weiner, Michael W., & Mattsson, Niklas. Time to Amyloid Positivity and Preclinical Changes in Brain Metabolism, Atrophy, and Cognition: Evidence for Emerging Amyloid Pathology in Alzheimer's Disease. United States. https://doi.org/10.3389/fnins.2017.00281
Insel, Philip S., Ossenkoppele, Rik, Gessert, Devon, Jagust, William, Landau, Susan, Hansson, Oskar, Weiner, Michael W., and Mattsson, Niklas. Wed .
"Time to Amyloid Positivity and Preclinical Changes in Brain Metabolism, Atrophy, and Cognition: Evidence for Emerging Amyloid Pathology in Alzheimer's Disease". United States. https://doi.org/10.3389/fnins.2017.00281. https://www.osti.gov/servlets/purl/1628204.
@article{osti_1628204,
title = {Time to Amyloid Positivity and Preclinical Changes in Brain Metabolism, Atrophy, and Cognition: Evidence for Emerging Amyloid Pathology in Alzheimer's Disease},
author = {Insel, Philip S. and Ossenkoppele, Rik and Gessert, Devon and Jagust, William and Landau, Susan and Hansson, Oskar and Weiner, Michael W. and Mattsson, Niklas},
abstractNote = {Background: Aβ pathology is associated with longitudinal changes of brain metabolism, atrophy, and cognition, in cognitively healthy elders. However, Aβ information is usually measured cross-sectionally and dichotomized to classify subjects as Aβ-positive or Aβ-negative, making it difficult to evaluate when brain and cognitive changes occur with respect to emerging Aβ pathology. In this study, we use longitudinal Aβ information to combine the level and rate of change of Aβ to estimate the time to Aβ-positivity for each subject and test this temporal proximity to significant Aβ pathology for associations with brain structure, metabolism, and cognition. Methods: In 89 cognitively healthy elders with up to 10 years of follow-up, we estimated the points at which rates of fluorodeoxyglucose (FDG) PET, MRI, and cognitive and functional decline begin to accelerate with respect to the time to Aβ-positivity. Points of initial acceleration in rates of decline were estimated using mixed-effects models with penalized regression splines. Results: Acceleration of rates of FDG PET were observed to occur 20+ years before the conventional threshold for Aβ-positivity. Subtle signs of cognitive dysfunction were observed 10+ years before Aβ-positivity. Conclusions: Aβ may have subtle associations with other hallmarks of Alzheimer’s disease before Aβ biomarkers reach conventional thresholds for Aβ-positivity. Therefore, we propose that emerging Aβ pathology occurs many years before cognitively healthy elders reach the current threshold for Aβ positivity (preclinical AD). To allow prevention in the earliest disease stages, AD clinical trials may be designed to also include subjects with Aβ biomarkers in the sub-threshold range.},
doi = {10.3389/fnins.2017.00281},
journal = {Frontiers in Neuroscience (Online)},
number = ,
volume = 11,
place = {United States},
year = {Wed May 17 00:00:00 EDT 2017},
month = {Wed May 17 00:00:00 EDT 2017}
}
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Independent information from cerebrospinal fluid amyloid-β and florbetapir imaging in Alzheimer's disease
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Cerebrospinal fluid analysis detects cerebral amyloid-β accumulation earlier than positron emission tomography
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Amyloid-first and neurodegeneration-first profiles characterize incident amyloid PET positivity
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Accelerating rates of cognitive decline and imaging markers associated with β-amyloid pathology
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