Amyloid Deposition Is Associated with Impaired Default Network Function in Older Persons without Dementia
Open accessAbstract
Alzheimer's disease (AD) has been associated with functional alterations in a distributed network of brain regions linked to memory function, with a recent focus on the cortical regions collectively known as the default network. Posterior components of the default network, including the precuneus and posterior cingulate, are particularly vulnerable to early deposition of amyloid beta-protein, one of the hallmark pathologies of AD. In this study, we use in vivo amyloid imaging to demonstrate that high levels of amyloid deposition are associated with aberrant default network functional magnetic resonance imaging (fMRI) activity in asymptomatic and minimally impaired older individuals, similar to the pattern of dysfunction reported in AD patients. These findings suggest that amyloid pathology is linked to neural dysfunction in brain regions supporting memory function and provide support for the hypothesis that cognitively intact older individuals with evidence of amyloid pathology may be in early stages of AD.
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
A certain overlap between the DMN and the distribution of Aβ fibrils in AD has been noted in previous publications.
“A certain overlap between the DMN and the distribution of Aβ fibrils in AD has also been noted in previous publications23–26.”
From Earliest accumulation of β-amyloid occurs within the default-mode network and concurrently affects brain connectivity (2017) · cites this paper as [24]
Sites of high cerebral activity in the default system are sites of early AD neuropathology, but not necessarily because of increased Aβ secretion.
“Another explanation for the potential Aβ/synaptic activity paradox is that sites of high cerebral activity, in the default system, are indeed sites of early AD neuropathology [18, 179], but not necessarily because of increased Aβ secretion.”
From Intraneuronal β-amyloid accumulation and synapse pathology in Alzheimer’s disease (2010) · cites this paper as [179]
Presence of plaques by PiB PET even in cognitively normal individuals reflects deficits on functional imaging.
“Furthermore, a recent imaging study supports that the presence of plaques by Pittsburgh compound B (PiB) PET amyloid imaging even in those diagnosed as cognitively normal does reflect deficits on functional imaging [179].”
From Intraneuronal β-amyloid accumulation and synapse pathology in Alzheimer’s disease (2010) · cites this paper as [179]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
The citation lists haven’t been fetched yet
References 75 · Cited by 1,027
Research works printed but not linked: 1
- Miller SL Fenstermacher E Bates J Blacker D Sperling RA Dickerson BC 2008b Hippocampal activation in adults with mild cognitive impairment predicts subsequent cognitive decline J Neurol Neurosurg Psychiatry 79 630 635 17846109 PMC2683145
- Authors
- Sperling, R. A., LaViolette, P. S., O'Keefe, K., O'Brien, J., Rentz, D. M., Pihlajamaki, M., Marshall, G., Hyman, B. T., Selkoe, D. J., Hedden, T., Buckner, R. L., Becker, J. A., & Johnson, K. A.
- Affiliations
- Brigham and Women's Hospital (US)
- Harvard University (US)
- Howard Hughes Medical Institute (US)
- Corresponding author
- Sperling, Reisa A.
- ORCID
- Venue
- Neuron
- Publisher
- Elsevier BV
- Published
- 2009-07
- Volume
- 63
- Issue
- 2
- Pages
- 178-188
- ISSN
- 0896-6273 (ISSN-L)
- PMC
- PMC2738994
- OpenAlex
- W1997301424
- Cited by
- 1,027
- References
- 75
- Citations by year
- 2026: 42 · 2025: 48 · 2024: 40 · 2023: 49 · 2022: 45 · 2021: 69 · 2020: 64 · 2019: 61 · 2018: 60 · 2017: 60 · 2016: 57 · 2015: 69 · 2014: 65 · 2013: 70 · 2012: 83
- FWCI
- 47.00
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 1477 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Neuron (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Howard Hughes Medical Institute
- Massachusetts General Hospital
- University of Pittsburgh
- Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital
- National Institute on Aging (R01AG021910, R01AG027435, P50AG005134, R01AG034556)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Cognitive Neuroscience › Functional Brain Connectivity Studies
- Keywords
- amyloid deposition, amyloid-beta, default mode network, Alzheimer's disease, precuneus, posterior cingulate cortex, functional MRI, older adults without dementia, memory function, early Alzheimer's disease, amyloid imaging
- MeSH terms
- Adult, Aged, Aged, 80 and over, Cognition, Dementia, Female, Hippocampus, Humans, Image Processing, Computer-Assisted, Magnetic Resonance Imaging, Male, Microscopy, Electron, Nerve Net, Neurons, Amyloid beta-Peptides
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review