Clinical, genetic, and neuropathologic characteristics of posterior cortical atrophy
Tang-Wai DF, Graff-Radford NR, Boeve BF, Dickson DW, Parisi JE, Crook R, Caselli RJ, Knopman DS et al.. Neurology, 2004-10-01
Topic: Brain proteins, microglia and lab models
Objective To examine the clinical, genetic, and neuropathologic features of posterior cortical atrophy (PCA). Design/methods Using a broad definition of PCA as a syndrome with the insidious onset of visual dysfunction in the absence of primary ophthalmologic causes, the authors identified and then reviewed the presenting signs and symptoms, ApoE genotypes, tau haplotypes, and neuropathologic findings when available of PCA cases from two dementia research centers collected over the past 14 years. Results The authors identified 40 PCA cases. Their mean age at symptom onset was 60.5 +/- 8.9 years. There were twice as many women as men in the series. The principal types of visual impairment were simultanagnosia (82%) and visual field defect (47.5%). Acalculia, alexia, and anomia were also common. Insight was preserved in almost all (95%) early in the disorder. Neither apoE epsilon4 nor tau haplotype frequencies were different from typical Alzheimer disease (AD). Nine patients had died and underwent postmortem examination. Seven autopsied cases had AD pathology but when compared to typical AD, the neurofibrillary tangle (NFT) densities were significantly higher in Brodmann areas 17 and 18 (p Conclusions PCA is a distinctive dementia syndrome in which the most pronounced pathologic involvement is in the occipitoparietal regions independent of the specific underlying pathology. AD was the most common pathologic cause, but its regional distribution differed from typical AD.
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APA 7th
Tang-Wai, D. F., Graff-Radford, N. R., Boeve, B. F., Dickson, D. W., Parisi, J. E., Crook, R., et al. (2004). Clinical, genetic, and neuropathologic characteristics of posterior cortical atrophy. Neurology. https://doi.org/10.1212/01.wnl.0000140289.18472.15
Vancouver
Tang-Wai DF, Graff-Radford NR, Boeve BF, Dickson DW, Parisi JE, Crook R, et al. Clinical, genetic, and neuropathologic characteristics of posterior cortical atrophy. Neurology. 2004. doi:10.1212/01.wnl.0000140289.18472.15. PMID: 15477533.
BibTeX
@article{tangwai2004-15477533,
author = {Tang-Wai, D. F. and Graff-Radford, N. R. and Boeve, B. F. and Dickson, D. W. and Parisi, J. E. and Crook, R. and Caselli, R. J. and Knopman, D. S. and others},
title = {{Clinical, genetic, and neuropathologic characteristics of posterior cortical atrophy}},
journal = {Neurology},
year = {2004},
doi = {10.1212/01.wnl.0000140289.18472.15},
pmid = {15477533},
url = {https://doi.org/10.1212/01.wnl.0000140289.18472.15}
}
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Key findings
- Results The authors identified 40 PCA cases.
- Seven autopsied cases had AD pathology but when compared to typical AD, the neurofibrillary tangle (NFT) densities were significantly higher in Brodmann areas 17 and 18 (p < 0.05) and significantly lower in the hippocampus (p < 0.05).
Why it matters
This review of 40 cases describes posterior cortical atrophy as a dementia syndrome with prominent occipitoparietal pathology, and seven autopsied cases had Alzheimer's pathology with higher tangle densities in visual brain areas than typical Alzheimer's disease. It is a descriptive case series and does not report a treatment, cure, or prevention.
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Study details
- Effect size47.5%
- Evidence strengthLow
How this study scored 53/100
Published in a leading specialty journal. Scored zero for study design, sample size, studied in people 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 | 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 | 2004 — older than 20 years, still counted |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 2 / 3 | Effect reported as a number, without an interval or test |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 6 / 7 | Cited 630 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 26.2 citations a year over 24 year(s) since 2004 |
| 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 27 other studies in this library |
| Still being cited | 3 / 4 | Cited 71 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Ronald Petersen: h-index 64 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | Mayo Clinic: institution h-index 1,606 (OpenAlex) |
| Multicenter collaboration | 0 / 3 | OpenAlex lists 1 institution(s) in 1 country — scores zero (affiliation lists can be incomplete) |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 15477533) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 53 / 100 | — |
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