Amyloid‐β associated cortical thinning in clinically normal elderly
Open accessAbstract
OBJECTIVE: Both amyloid-β (Aβ) deposition and brain atrophy are associated with Alzheimer's disease (AD) and the disease process likely begins many years before symptoms appear. We sought to determine whether clinically normal (CN) older individuals with Aβ deposition revealed by positron emission tomography (PET) imaging using Pittsburgh Compound B (PiB) also have evidence of both cortical thickness and hippocampal volume reductions in a pattern similar to that seen in AD. METHODS: A total of 119 older individuals (87 CN subjects and 32 patients with mild AD) underwent PiB PET and high-resolution structural magnetic resonance imaging (MRI). Regression models were used to relate PiB retention to cortical thickness and hippocampal volume. RESULTS: We found that PiB retention in CN subjects was (1) age-related and (2) associated with cortical thickness reductions, particularly in parietal and posterior cingulate regions extending into the precuneus, in a pattern similar to that observed in mild AD. Hippocampal volume reduction was variably related to Aβ deposition. INTERPRETATION: We conclude that Aβ deposition is associated with a pattern of cortical thickness reduction consistent with AD prior to the development of cognitive impairment.
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It is well established that the pathological burden of diverse lesions and proteinopathies can be substantial in people who are living independently and are clinically asymptomatic.
“it is well established that the pathological burden of diverse lesions and proteinopathies can be substantial in people who are living independently and are clinically asymptomatic [103–107].”
From The Need to Separate Chronic Traumatic Encephalopathy Neuropathology from Clinical Features (2017) · cites this paper as [106]
The Introduction reports that 25–50% of clinically normal older individuals exhibit amyloid-β deposition, and the Interpretation associates that deposition with cortical thinning before cognitive impairment. This supports substantial pathology without clinical symptoms, but the paper does not establish a burden of diverse lesions and proteinopathies or state that the participants lived independently. (LLM, conf=0.85)
Experimental — accuracy not yet measuredThe correlation between hallmark lesions and the presence and severity of disease is modest.
“the correlation between hallmark lesions and the presence and severity of disease is modest”
From The Need to Separate Chronic Traumatic Encephalopathy Neuropathology from Clinical Features (2017) · cites this paper as [106]
The Introduction reports that amyloid-β can accumulate before symptoms and plateaus as dementia emerges; it also notes amyloid deposition in clinically normal older people. This supports an imperfect relationship between amyloid and clinical disease, but the paper does not establish that the correlation is modest for hallmark lesions generally, including neurofibrillary tangles. Page numbers are not available in our copy. (LLM, conf=0.82)
Experimental — accuracy not yet measuredReduced plaque formation could have a role in preventing further cortical atrophy in AD brain, as plaque deposition has been correlated with accelerated cortical atrophy.
“reduced plaque formation could have a role in preventing further cortical atrophy in AD brain, as plaque deposition in multiple studies has been correlated with accelerated cortical atrophy [58], [59].”
From Galantamine Slows Down Plaque Formation and Behavioral Decline in the 5XFAD Mouse Model of Alzheimer’s Disease (2014) · cites this paper as [58]
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References 76 · Cited by 342
Research works printed but not linked: 1
- [4]Mintun MA Larossa GN Sheline YI [11C]PIB in a nondemented population: potential antecedent marker of Alzheimer disease Neurology 2006 67 446 452 16894106
- Authors
- Becker, J. A., Hedden, T., Carmasin, J., Maye, J., Rentz, D. M., Putcha, D., Fischl, B., Greve, D. N., Marshall, G. A., Salloway, S., Marks, D., Buckner, R. L., Sperling, R. A., & Johnson, K. A.
- Affiliations
- Harvard University (US)
- Brigham and Women's Hospital (US)
- Brown University (US)
- Tufts University (US)
- Howard Hughes Medical Institute (US)
- Corresponding author
- Johnson, Keith A.
- ORCID
- Venue
- Annals of Neurology
- Publisher
- Wiley
- Published
- 2011-03-17
- Volume
- 69
- Issue
- 6
- Pages
- 1032-1042
- ISSN
- 0364-5134 (ISSN-L)
- 1531-8249
- PMC
- PMC3117980
- OpenAlex
- W2098580427
- Cited by
- 342
- References
- 76
- Citations by year
- 2026: 8 · 2025: 11 · 2024: 12 · 2023: 13 · 2022: 13 · 2021: 18 · 2020: 31 · 2019: 22 · 2018: 24 · 2017: 22 · 2016: 18 · 2015: 27 · 2014: 38 · 2013: 34 · 2012: 31
- FWCI
- 18.26
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Annals of Neurology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- Howard Hughes Medical Institute
- Rosalinde and Arthur Gilbert Foundation
- National Institutes of Health (AG 036694)
- National Institute on Aging (AG021910, AG036694, R01AG021910, K24AG035007, P50-AG00513421, R01AG027435, R01AG037497, P50AG005134, K23AG033634, R01AG034556, P01AG036694)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Cancer-related cognitive impairment studies
- Keywords
- amyloid-beta deposition, cortical thinning, cortical thickness, hippocampal volume, Alzheimer's disease, Pittsburgh compound B, amyloid PET, brain atrophy, precuneus, posterior cingulate cortex, parietal cortex, mild Alzheimer's disease, preclinical Alzheimer's disease
- MeSH terms
- Age Factors, Aged, Aged, 80 and over, Aging, Alzheimer Disease, Analysis of Variance, Aniline Compounds, Brain Mapping, Cerebral Cortex, Female, Hippocampus, Humans, Magnetic Resonance Imaging, Male, Middle Aged, Statistics as Topic, Thiazoles, Amyloid beta-Peptides, Positron-Emission Tomography
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