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Imaging amyloid deposition in Lewy body diseases
Gomperts SN, Rentz DM, Moran E, Becker JA, Locascio JJ, Klunk WE, Mathis CA, Elmaleh DR et al.. Neurology, 2008-09-01
Topic: Amyloid, tau and blood-test diagnosis
Background Extrapyramidal motor symptoms precede dementia in Parkinson disease (PDD) by many years, whereas dementia occurs early in dementia with Lewy bodies (DLB). Despite this clinical distinction, the neuropsychological and neuropathologic features of these conditions overlap. In addition to widespread distribution of Lewy bodies, both diseases have variable burdens of neuritic plaques and neurofibrillary tangles characteristic of Alzheimer disease (AD). Objectives To determine whether amyloid deposition, as assessed by PET imaging with the beta-amyloid-binding compound Pittsburgh Compound B (PiB), can distinguish DLB from PDD, and to assess whether regional patterns of amyloid deposition correlate with specific motor or cognitive features. Methods Eight DLB, 7 PDD, 11 Parkinson disease (PD), 15 AD, and 37 normal control (NC) subjects underwent PiB-PET imaging and neuropsychological assessment. Amyloid burden was quantified using the PiB distribution volume ratio. Results Cortical amyloid burden was higher in the DLB group than in the PDD group, comparable to the AD group. Amyloid deposition in the PDD group was low, comparable to the PD and NC groups. Relative to global cortical retention, occipital PiB retention was lower in the AD group than in the other groups. For the DLB, PDD, and PD groups, amyloid deposition in the parietal (lateral and precuneus)/posterior cingulate region was related to visuospatial impairment. Striatal PiB retention in the DLB and PDD groups was associated with less impaired motor function. Conclusions Global cortical amyloid burden is high in dementia with Lewy bodies (DLB) but low in Parkinson disease dementia. These data suggest that beta-amyloid may contribute selectively to the cognitive impairment of DLB and may contribute to the timing of dementia relative to the motor signs of parkinsonism.
Key findings
- Results Cortical amyloid burden was higher in the DLB group than in the PDD group, comparable to the AD group.
- Striatal PiB retention in the DLB and PDD groups was associated with less impaired motor function.
- These data suggest that beta-amyloid may contribute selectively to the cognitive impairment of DLB and may contribute to the timing of dementia relative to the motor signs of parkinsonism.
Why it matters
In a PET study of 78 people, including 8 with dementia with Lewy bodies (DLB) and 7 with Parkinson disease dementia (PDD), cortical amyloid was high in DLB, comparable to Alzheimer's disease, but low in PDD, comparable to Parkinson's without dementia and healthy controls. The authors suggest amyloid "may contribute selectively to the cognitive impairment of DLB" and to when dementia appears relative to movement symptoms. This is a one-time comparison of small groups, so it cannot show that amyloid causes dementia, and it is not a test for diagnosing an individual patient.
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Study details
- Evidence strengthLow
How this study scored 57/100
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 | 2008 — 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 | 6 / 7 | Cited 444 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 22.2 citations a year over 20 year(s) since 2008 |
| Impact for its field and year | 5 / 6 | Cited 26.8× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 4 / 6 | Cited by 43 other studies in this library |
| Still being cited | 2 / 4 | Cited 16 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 4 / 4 | Last-listed author Keith A. Johnson: h-index 127 (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 18794492) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 57 / 100 | — |
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Read the original
- DOI: 10.1212/01.wnl.0000326146.60732.d6
- PubMed: 18794492
- 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).
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
Gomperts, S. N., Rentz, D. M., Moran, E., Becker, J. A., Locascio, J. J., Klunk, W. E., et al. (2008). Imaging amyloid deposition in Lewy body diseases. Neurology. https://doi.org/10.1212/01.wnl.0000326146.60732.d6
Vancouver
Gomperts SN, Rentz DM, Moran E, Becker JA, Locascio JJ, Klunk WE, et al. Imaging amyloid deposition in Lewy body diseases. Neurology. 2008. doi:10.1212/01.wnl.0000326146.60732.d6. PMID: 18794492.
BibTeX
@article{gomperts2008-18794492,
author = {Gomperts, S. N. and Rentz, D. M. and Moran, E. and Becker, J. A. and Locascio, J. J. and Klunk, W. E. and Mathis, C. A. and Elmaleh, D. R. and others},
title = {{Imaging amyloid deposition in Lewy body diseases}},
journal = {Neurology},
year = {2008},
doi = {10.1212/01.wnl.0000326146.60732.d6},
pmid = {18794492},
url = {https://doi.org/10.1212/01.wnl.0000326146.60732.d6}
}
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