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Impaired default network functional connectivity in autosomal dominant Alzheimer disease
Chhatwal JP, Schultz AP, Johnson K, Benzinger TL, Jack C, Ances BM, Sullivan CA, Salloway SP et al.. Neurology, 2013-07-24
Topic: Amyloid, tau and blood-test diagnosis
Objective To investigate default mode network (DMN) functional connectivity MRI (fcMRI) in a large cross-sectional cohort of subjects from families harboring pathogenic presenilin-1 (PSEN1), presenilin-2 (PSEN2), and amyloid precursor protein (APP) mutations participating in the Dominantly Inherited Alzheimer Network. Methods Eighty-three mutation carriers and 37 asymptomatic noncarriers from the same families underwent fMRI during resting state at 8 centers in the United States, United Kingdom, and Australia. Using group-independent component analysis, fcMRI was compared using mutation status and Clinical Dementia Rating to stratify groups, and related to each participant's estimated years from expected symptom onset (eYO). Results We observed significantly decreased DMN fcMRI in mutation carriers with increasing Clinical Dementia Rating, most evident in the precuneus/posterior cingulate and parietal cortices (p Conclusion Functional disruption of the DMN occurs early in the course of autosomal dominant Alzheimer disease, beginning before clinically evident symptoms, and worsening with increased impairment. These findings suggest that DMN fcMRI may prove useful as a biomarker across a wide spectrum of disease, and support the feasibility of DMN fcMRI as a secondary endpoint in upcoming multicenter clinical trials in Alzheimer disease.
Key findings
- Results We observed significantly decreased DMN fcMRI in mutation carriers with increasing Clinical Dementia Rating, most evident in the precuneus/posterior cingulate and parietal cortices (p < 0.001).
- These findings suggest that DMN fcMRI may prove useful as a biomarker across a wide spectrum of disease, and support the feasibility of DMN fcMRI as a secondary endpoint in upcoming multicenter clinical trials in Alzheimer disease.
Why it matters
In people with inherited mutations causing early Alzheimer disease, brain network connectivity was reduced even before symptoms appeared and worsened with greater impairment. This imaging measure may be useful as a marker in future trials, but it is not itself a treatment or cure.
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Study details
- Study designcross-sectional
- Evidence strengthModerate
How this study scored 58/100
Published in a leading specialty journal, and it is a snapshot of people at one point in time. Scored zero for 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 | 4 / 12 | A snapshot of people at one point in time |
| Strength of evidence | 3 / 5 | Rated “moderate” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 1 / 5 | 2013 — 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 179 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 11.9 citations a year over 15 year(s) since 2013 |
| Impact for its field and year | 3 / 6 | Cited 7.9× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 3 / 6 | Cited by 11 other studies in this library |
| Still being cited | 2 / 4 | Cited 17 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 4 / 4 | Last-listed author Reisa Anne Sperling: h-index 157 (OpenAlex, whole career) |
| Institution's track record | 3 / 3 | Harvard University: institution h-index 3,235 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | PubMed indexes it as a multicentre study |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 23884042) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 58 / 100 | — |
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Read the original
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. The record's author list ends in “et al.”, so not every author is named. Check the citation against the original before you use it.
APA 7th
Chhatwal, J. P., Schultz, A. P., Johnson, K., Benzinger, T. L., Jack, C., Ances, B. M., et al. (2013). Impaired default network functional connectivity in autosomal dominant Alzheimer disease. Neurology. https://doi.org/10.1212/wnl.0b013e3182a1aafe
Vancouver
Chhatwal JP, Schultz AP, Johnson K, Benzinger TL, Jack C, Ances BM, et al. Impaired default network functional connectivity in autosomal dominant Alzheimer disease. Neurology. 2013. doi:10.1212/wnl.0b013e3182a1aafe. PMID: 23884042.
BibTeX
@article{chhatwal2013-23884042,
author = {Chhatwal, J. P. and Schultz, A. P. and Johnson, K. and Benzinger, T. L. and Jack, C. and Ances, B. M. and Sullivan, C. A. and Salloway, S. P. and others},
title = {{Impaired default network functional connectivity in autosomal dominant Alzheimer disease}},
journal = {Neurology},
year = {2013},
doi = {10.1212/wnl.0b013e3182a1aafe},
pmid = {23884042},
url = {https://doi.org/10.1212/wnl.0b013e3182a1aafe}
}
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