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MRI cortical thickness biomarker predicts AD-like CSF and cognitive decline in normal adults
Dickerson BC, Wolk DA, Alzheimer's Disease Neuroimaging Initiative.. Neurology, 2011-12-21
Topic: Amyloid, tau and blood-test diagnosis
Objective New preclinical Alzheimer disease (AD) diagnostic criteria have been developed using biomarkers in cognitively normal (CN) adults. We implemented these criteria using an MRI biomarker previously associated with AD dementia, testing the hypothesis that individuals at high risk for preclinical AD would be at elevated risk for cognitive decline. Methods The Alzheimer's Disease Neuroimaging Initiative database was interrogated for CN individuals. MRI data were processed using a published set of a priori regions of interest to derive a single measure known as the AD signature (ADsig). Each individual was classified as ADsig-low (≥ 1 SD below the mean: high risk for preclinical AD), ADsig-average (within 1 SD of mean), or ADsig-high (≥ 1 SD above mean). A 3-year cognitive decline outcome was defined a priori using change in Clinical Dementia Rating sum of boxes and selected neuropsychological measures. Results Individuals at high risk for preclinical AD were more likely to experience cognitive decline, which developed in 21% compared with 7% of ADsig-average and 0% of ADsig-high groups (p = 0.03). Logistic regression demonstrated that every 1 SD of cortical thinning was associated with a nearly tripled risk of cognitive decline (p = 0.02). Of those for whom baseline CSF data were available, 60% of the high risk for preclinical AD group had CSF characteristics consistent with AD while 36% of the ADsig-average and 19% of the ADsig-high groups had such CSF characteristics (p = 0.1). Conclusions This approach to the detection of individuals at high risk for preclinical AD-identified in single CN individuals using this quantitative ADsig MRI biomarker-may provide investigators with a population enriched for AD pathobiology and with a relatively high likelihood of imminent cognitive decline consistent with prodromal AD.
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APA 7th
Dickerson, B. C., Wolk, D. A., & Alzheimer's Disease Neuroimaging Initiative. (2012). MRI cortical thickness biomarker predicts AD-like CSF and cognitive decline in normal adults. Neurology. https://doi.org/10.1212/wnl.0b013e31823efc6c
Vancouver
Dickerson BC, Wolk DA, Alzheimer's Disease Neuroimaging Initiative. MRI cortical thickness biomarker predicts AD-like CSF and cognitive decline in normal adults. Neurology. 2012. doi:10.1212/wnl.0b013e31823efc6c. PMID: 22189451.
BibTeX
@article{dickerson2012-22189451,
author = {Dickerson, B. C. and Wolk, D. A. and {Alzheimer's Disease Neuroimaging Initiative}},
title = {{MRI cortical thickness biomarker predicts AD-like CSF and cognitive decline in normal adults}},
journal = {Neurology},
year = {2012},
doi = {10.1212/wnl.0b013e31823efc6c},
pmid = {22189451},
url = {https://doi.org/10.1212/wnl.0b013e31823efc6c}
}
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Key findings
- We implemented these criteria using an MRI biomarker previously associated with AD dementia, testing the hypothesis that individuals at high risk for preclinical AD would be at elevated risk for cognitive decline.
- Results Individuals at high risk for preclinical AD were more likely to experience cognitive decline, which developed in 21% compared with 7% of ADsig-average and 0% of ADsig-high groups (p = 0.03).
- Logistic regression demonstrated that every 1 SD of cortical thinning was associated with a nearly tripled risk of cognitive decline (p = 0.02).
Why it matters
Among cognitively normal adults, those with an MRI cortical thickness pattern linked to Alzheimer disease were more likely to decline cognitively over three years (21% versus 7% and 0%). This supports the marker for identifying preclinical risk, but it does not show any way to prevent the decline.
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Study details
- Evidence strengthLow
How this study scored 53/100
Published in a leading specialty journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 9 / 10 | Tier 2 — leading specialty journal (Neurology) |
| Journal's citation record | 4 / 4 | Neurology: journal h-index 525 (OpenAlex, 2026-10-29) |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 1 / 5 | 2012 — within 20 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 5 / 7 | Cited 240 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 15.0 citations a year over 16 year(s) since 2012 |
| Impact for its field and year | 4 / 6 | Cited 12.3× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 3 / 6 | Cited by 16 other studies in this library |
| Still being cited | 3 / 4 | Cited 50 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author David A. Wolk: h-index 96 (OpenAlex, whole career) |
| Institution's track record | 3 / 3 | Harvard University: institution h-index 3,235 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 4 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 22189451) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 53 / 100 | — |
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