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This page is alzhub.org's plain-English summary of a published study, not the paper itself. It is generated from the record we hold for this study, sourced and linked below — check the original for the full text and methods.

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Getting a diagnosis

Topic: Risk, prevention and care in population studies

Objective To characterize cognitive and behavioral features, physical findings, and brain atrophy patterns in pathology-proven corticobasal degeneration (CBD) and corticobasal syndrome (CBS) with known histopathology. Methods We reviewed clinical and magnetic resonance imaging data in all patients evaluated at our center with either an autopsy diagnosis of CBD (n = 18) or clinical CBS at first presentation with known histopathology (n = 40). Atrophy patterns were compared using voxel-based morphometry. Results CBD was associated with 4 clinical syndromes: progressive nonfluent aphasia (n = 5), behavioral variant frontotemporal dementia (n = 5), executive-motor (n = 7), and posterior cortical atrophy (n = 1). Behavioral or cognitive problems were the initial symptoms in 15 of 18 patients; less than half exhibited early motor findings. Compared to controls, CBD patients showed atrophy in dorsal prefrontal and perirolandic cortex, striatum, and brainstem (p Interpretation Frontal lobe involvement is characteristic of CBD, and in many patients frontal, not parietal or basal ganglia, symptoms dominate early stage disease. CBS is driven by medial perirolandic dysfunction, but this anatomy is not specific to a single underlying histopathology. Antemortem prediction of CBD will remain challenging until clinical features of CBD are redefined, and sensitive, specific biomarkers are identified.

Key findings

Why it matters

This study found that pathology-proven corticobasal degeneration was associated with several clinical syndromes and that frontal lobe involvement is characteristic, making antemortem prediction challenging. It is about diagnosing corticobasal degeneration, not about treating, curing, or preventing Alzheimer's disease.

Study details

How this study scored 57/100
How this study's score is builtJournal tier 9 of 10; Journal's citation record 3 of 4; Study design 0 of 12; Strength of evidence 1 of 5; Peer-review validation 10 of 10; How recent 1 of 5; Sample size 1 of 4; Effect reported 0 of 3; Studied in people 3 of 3; Randomised / blinded 0 of 2; Times cited 6 of 7; Citations per year 4 of 5; Impact for its field and year 4 of 6; Cited by studies here 3 of 6; Still being cited 3 of 4; Senior author's track record 4 of 4; Institution's track record 2 of 3; Multi-centre collaboration 1 of 3; Indexed in PubMed 2 of 2; Free to read 0 of 2. Total 57 of 100.57 of 100 points earned43 not earned

Published in a leading specialty journal. Scored zero for study design, effect reported and randomised / blinded because the record does not state it.

ComponentPointsWhy
Journal tier 9 / 10 Tier 2 — leading specialty journal (Annals of neurology)
Journal's citation record 3 / 4 Annals of Neurology: journal h-index 437 (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 2011 — within 20 year(s) of the newest study here
Sample size 1 / 4 18 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)
Randomised / blinded 0 / 2 No randomisation or blinding stated — scores zero (not stated in the record — scored 0)
Times cited 6 / 7 Cited 438 times (OpenAlex, 2026-10-10)
Citations per year 4 / 5 25.8 citations a year over 17 year(s) since 2011
Impact for its field and year 4 / 6 Cited 16.2× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here 3 / 6 Cited by 26 other studies in this library
Still being cited 3 / 4 Cited 66 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record 4 / 4 Last-listed author Bruce L. Miller: h-index 198 (OpenAlex, whole career)
Institution's track record 2 / 3 University of California, San Francisco: institution h-index 1,915 (OpenAlex)
Multi-centre collaboration 1 / 3 OpenAlex lists 3 institution(s) in 1 country
Indexed in PubMed 2 / 2 Indexed in PubMed (PMID 21823158)
Free to read 0 / 2 Behind a paywall — scores zero
Total 57 / 100 —

What each of these 20 components measures, and what this score is not →

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

Lee, S. E., Rabinovici, G. D., Mayo, M. C., Wilson, S. M., Seeley, W. W., DeArmond, S. J., et al. (2011). Clinicopathological correlations in corticobasal degeneration. Annals of neurology. https://doi.org/10.1002/ana.22424

Vancouver

Lee SE, Rabinovici GD, Mayo MC, Wilson SM, Seeley WW, DeArmond SJ, et al. Clinicopathological correlations in corticobasal degeneration. Annals of neurology. 2011. doi:10.1002/ana.22424. PMID: 21823158.

BibTeX

@article{lee2011-21823158,
  author  = {Lee, S. E. and Rabinovici, G. D. and Mayo, M. C. and Wilson, S. M. and Seeley, W. W. and DeArmond, S. J. and Huang, E. J. and Trojanowski, J. Q. and others},
  title   = {{Clinicopathological correlations in corticobasal degeneration}},
  journal = {Annals of neurology},
  year    = {2011},
  doi     = {10.1002/ana.22424},
  pmid    = {21823158},
  url     = {https://doi.org/10.1002/ana.22424}
}

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