Emerging β-amyloid pathology and accelerated cortical atrophy
Open accessAbstract
IMPORTANCE: The effect of β-amyloid (Aβ) accumulation on regional structural brain changes in early stages of Alzheimer disease (AD) is not well understood. OBJECTIVE: To test the hypothesis that the development of Aβ pathology is related to increased regional atrophy in the brains of cognitively normal (CN) persons. DESIGN, SETTING, AND PARTICIPANTS: Longitudinal clinicobiomarker cohort study involving 47 CN control subjects and 15 patients with AD dementia. All participants underwent repeated cerebrospinal fluid Aβ42 and structural magnetic resonance imaging measurements for up to 4 years. Cognitively normal controls were classified using the longitudinal cerebrospinal fluid Aβ42 data and included 13 stable Aβ negative (normal baseline Aβ42 levels, with less than the median reduction over time), 13 declining Aβ negative (normal baseline Aβ42 levels, with greater than the median reduction over time), and 21 Aβ positive (pathologic baseline Aβ42 levels). All 15 patients with AD dementia were Aβ positive. MAIN OUTCOMES AND MEASURES: Group effects on regional gray matter volumes at baseline and over time, tested by linear mixed-effects models. RESULTS: Baseline gray matter volumes were similar among the CN Aβ groups, but atrophy rates were increased in frontoparietal regions in the declining Aβ-negative and Aβ-positive groups and in amygdala and temporal regions in the Aβ-positive group. Aβ-positive patients with AD dementia had further increased atrophy rates in hippocampus and temporal and cingulate regions. CONCLUSIONS AND RELEVANCE: Emerging Aβ pathology is coupled to increased frontoparietal (but not temporal) atrophy rates. Atrophy rates peak early in frontoparietal regions but accelerate in hippocampus, temporal, and cingulate regions as the disease progresses to dementia. Early-stage Aβ pathology may have mild effects on local frontoparietal cortical integrity while effects in temporal regions appear later and accelerate, leading to the atrophy pattern typically seen in AD.
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Agitation in Alzheimer's disease is associated with core Alzheimer's disease disease progression.
“First, there are structural and functional deficits in a number of brain regions that are also implicated in the distribution of core AD pathology including PCC and hippocampus (Mattsson et al., 2014), suggesting an association between the core processes of AD disease progression and agitation.”
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- Authors
- Mattsson, N., Insel, P. S., Nosheny, R., Tosun, D., Trojanowski, J. Q., Shaw, L. M., Jack, C. R., Donohue, M. C., & Weiner, M. W.
- Affiliations
- San Francisco VA Medical Center (US)
- University of Pennsylvania (US)
- Mayo Clinic (US)
- University of California San Diego (US)
- ORCID
- Venue
- JAMA Neurology
- Publisher
- American Medical Association (AMA)
- Published
- 2014-06-01
- Volume
- 71
- Issue
- 6
- Pages
- 725
- ISSN
- 2168-6149 (ISSN-L)
- PMC
- PMC4410966
- OpenAlex
- W1987777001
- Cited by
- 71
- References
- 61
- Citations by year
- 2026: 3 · 2025: 11 · 2024: 5 · 2023: 4 · 2022: 5 · 2021: 2 · 2020: 4 · 2019: 6 · 2018: 3 · 2017: 8 · 2016: 10 · 2015: 7 · 2014: 3
- FWCI
- 7.12
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- JAMA Neurology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- U.S. Department of Defense (AG024904)
- Foundation for the National Institutes of Health (AG024904)
- U.S. Department of Veterans Affairs
- Alzheimer's Association (AG010129)
- Bristol-Myers Squibb (AG024904)
- Alzheimer's Drug Discovery Foundation
- Eli Lilly and Company (AG024904)
- Pfizer (AG024904)
- AstraZeneca
- GlaxoSmithKline
- Novartis
- F. Hoffmann-La Roche (AG024904)
- Medpace
- Synarc
- Alzheimer's Disease Neuroimaging Initiative (U01AG024904, AG024904)
- Danone
- Northern California Institute for Research and Education
- Elan
- Eisai (AG024904)
- Vetenskapsrådet
- Sahlgrenska Universitetssjukhuset
- National Institutes of Health (5u01ag024904-10, U01-AG024904, AG010129, AG024904, grants P30-AG010129)
- Genentech (AG024904)
- University of California, Los Angeles
- University of California, San Diego
- National Institute on Aging (U01-AG-024904, P30AG010129, AG 024904, K01AG030514, P30AG010124, AG010129, R01AG011378, R01AG037551, U01AG032438, R01AG041851)
- National Heart, Lung, and Blood Institute (U01HL096917)
- National Institute of Biomedical Imaging and Bioengineering (AG024904)
- 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 › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- amyloid-beta pathology, Alzheimer's disease, cortical atrophy, gray matter volume, hippocampal atrophy, amygdala, temporal lobe, cingulate cortex, early Alzheimer's disease, cognitively normal older adults, longitudinal neuroimaging
- MeSH terms
- Aged, Aged, 80 and over, Alzheimer Disease, Atrophy, Female, Humans, Longitudinal Studies, Magnetic Resonance Imaging, Male, Middle Aged, Peptide Fragments, Cohort Studies, Amyloid beta-Peptides, Disease Progression
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 ›
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