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Longitudinal volumetric MRI change and rate of cognitive decline
Mungas D, Harvey D, Reed BR, Jagust WJ, DeCarli C, Beckett L, Mack WJ, Kramer JH et al.. Neurology, 2005-08-01
Topic: Risk, prevention and care in population studies
Plain-language summary
Objective To examine how baseline and change of volumetric MRI relate to cognitive decline in older individuals. Background Memory is associated with hippocampal integrity, whereas executive function has been linked to impaired frontal lobe function. Previous studies have shown that hippocampal and cortical atrophy are more strongly related to cognition than are measures of subcortical cerebrovascular disease (CVD). The authors hypothesized that memory (MEM) decline would be related to change in hippocampal volume (HC), whereas decline in executive function (EXEC) would be related to change of cortical gray matter volume (CGM) and measures of subcortical CVD. Methods Subjects from a multicenter study (n = 103) included cognitively normal, mildly impaired, and demented cases with and without subcortical lacunes. All had longitudinal cognitive evaluation (mean = 4.8 years) and two or more MRI scans at least one year apart (mean = 3.4 years). MRI measures included HC, CGM, total lacune volume (LAC), and white matter hyperintensity volume (WMH). Random effects modeling of longitudinal data assessed effects of MRI baseline and MRI change on baseline and change of psychometrically matched measures of MEM and EXEC. Results Change in MEM was related to HC baseline and HC change. Change in EXEC was related to baseline CGM and to change in CGM, HC, and LAC. Results were unchanged when demented cases were excluded. WMH was not associated with change in MEM or EXEC independent of HC, CGM, and LAC. Conclusion Hippocampal volume was the primary determinant of memory decline, whereas executive function (EXEC) decline was related to multiple brain components. Results support a hypothesis that MEM decline is strongly influenced by Alzheimer disease (AD), whereas EXEC decline may be complexly determined by cerebrovascular disease and AD.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Mungas, D., Harvey, D., Reed, B. R., Jagust, W. J., DeCarli, C., Beckett, L., et al. (2005). Longitudinal volumetric MRI change and rate of cognitive decline. Neurology. https://doi.org/10.1212/01.wnl.0000172913.88973.0d
Vancouver
Mungas D, Harvey D, Reed BR, Jagust WJ, DeCarli C, Beckett L, et al. Longitudinal volumetric MRI change and rate of cognitive decline. Neurology. 2005. doi:10.1212/01.wnl.0000172913.88973.0d. PMID: 16116117.
BibTeX
@article{mungas2005-16116117,
author = {Mungas, D. and Harvey, D. and Reed, B. R. and Jagust, W. J. and DeCarli, C. and Beckett, L. and Mack, W. J. and Kramer, J. H. and others},
title = {{Longitudinal volumetric MRI change and rate of cognitive decline}},
journal = {Neurology},
year = {2005},
doi = {10.1212/01.wnl.0000172913.88973.0d},
pmid = {16116117},
url = {https://doi.org/10.1212/01.wnl.0000172913.88973.0d}
}
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Key findings
- Background Memory is associated with hippocampal integrity, whereas executive function has been linked to impaired frontal lobe function.
- Previous studies have shown that hippocampal and cortical atrophy are more strongly related to cognition than are measures of subcortical cerebrovascular disease (CVD).
- Results Change in MEM was related to HC baseline and HC change.
- Results were unchanged when demented cases were excluded.
- WMH was not associated with change in MEM or EXEC independent of HC, CGM, and LAC.
Why it matters
In 103 participants followed for about five years, memory decline was related to baseline hippocampal volume and its change, while executive function decline was related to cortical gray matter and other measures. This observational study describes how brain shrinkage tracks with cognitive decline but does not test any treatment or show that preventing shrinkage would change the disease course.
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Study details
- Study designlongitudinal study
- Participants103
- Evidence strengthModerate
How this study scored 66/100
Published in a leading specialty journal, and it is a longitudinal study following the same people over time. Scored zero for effect reported and randomized / 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 | 7 / 12 | A longitudinal study following the same people over 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 | 2005 — older than 20 years, still counted |
| Sample size | 2 / 4 | 103 participants |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 3 / 3 | Studied in people (participant count stated) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 6 / 7 | Cited 311 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 13.5 citations a year over 23 year(s) since 2005 |
| Impact for its field and year | 4 / 6 | Cited 12.1× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 3 / 6 | Cited by 24 other studies in this library |
| Still being cited | 2 / 4 | Cited 23 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Helena Chang Chui: h-index 93 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | University of California, Berkeley: institution h-index 2,012 (OpenAlex) |
| Multicenter collaboration | 2 / 3 | PubMed indexes it as a multicentre study |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 16116117) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 66 / 100 | — |
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Read the original
- DOI: 10.1212/01.wnl.0000172913.88973.0d
- PubMed: 16116117
- Original source →
- Free full text: PubMed Central →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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