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Beta Amyloid Deposition Is Not Associated With Cognitive Impairment in Parkinson's Disease
Melzer TR, Stark MR, Keenan RJ, Myall DJ, MacAskill MR, Pitcher TL, Livingston L, Grenfell S et al.. Frontiers in neurology, 2019-04-24
Topic: Amyloid, tau and blood-test diagnosis
The extent to which Alzheimer neuropathology, particularly the accumulation of misfolded beta-amyloid, contributes to cognitive decline and dementia in Parkinson's disease (PD) is unresolved. Here, we used Florbetaben PET imaging to test for any association between cerebral amyloid deposition and cognitive impairment in PD, in a sample enriched for cases with mild cognitive impairment. This cross-sectional study used Movement Disorders Society level II criteria to classify 115 participants with PD as having normal cognition (PDN, n = 23), mild cognitive impairment (PD-MCI, n = 76), or dementia (PDD, n = 16). We acquired 18F-Florbetaben (FBB) amyloid PET and structural MRI. Amyloid deposition was assessed between the three cognitive groups, and also across the whole sample using continuous measures of both global cognitive status and average performance in memory domain tests. Outcomes were cortical FBB uptake, expressed in centiloids and as standardized uptake value ratios (SUVR) using the Centiloid Project whole cerebellum region as a reference, and regional SUVR measurements. FBB binding was higher in PDD, but this difference did not survive adjustment for the older age of the PDD group. We established a suitable centiloid cut-off for amyloid positivity in Parkinson's disease (31.3), but there was no association of FBB binding with global cognitive or memory scores. The failure to find an association between PET amyloid deposition and cognitive impairment in a moderately large sample, particularly given that it was enriched with PD-MCI patients at risk of dementia, suggests that amyloid pathology is not the primary driver of cognitive impairment and dementia in most patients with PD.
Key findings
- The failure to find an association between PET amyloid deposition and cognitive impairment in a moderately large sample, particularly given that it was enriched with PD-MCI patients at risk of dementia, suggests that amyloid pathology is not the primary driver of cognitive impairment and dementia in most patients with PD.
Why it matters
This cross-sectional study of 115 people with Parkinson's disease found no association between amyloid PET binding and cognitive or memory scores, and the higher binding in the dementia group did not survive adjustment for age. The authors conclude that amyloid pathology is not the primary driver of cognitive impairment and dementia in Parkinson's disease.
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Study details
- Study designcross-sectional
- Participants23
- Evidence strengthLow
How this study scored 53/100
Published in a peer-reviewed journal, and it is a snapshot of people at one point in time. Scored zero for effect reported and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Frontiers in neurology) |
| Journal's citation record | 2 / 4 | Frontiers in Neurology: journal h-index 162 (OpenAlex, 2026-10-29) |
| Study design | 4 / 12 | A snapshot of people at one point in time |
| 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 | 2 / 5 | 2019 — within 10 year(s) of the newest study here |
| Sample size | 1 / 4 | 23 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 | 4 / 7 | Cited 81 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 9.0 citations a year over 9 year(s) since 2019 |
| 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 | 1 / 6 | Cited by 2 other studies in this library |
| Still being cited | 2 / 4 | Cited 22 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Tim Anderson: h-index 48 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | University College London: institution h-index 2,029 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 9 institution(s) in 3 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 31105633) |
| Free to read | 2 / 2 | Free to read |
| Total | 53 / 100 | — |
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Read the original
Full text: free to read — PubMed Central lists this copy as free to read: the link above (checked 10 Oct 2026).
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
Melzer, T. R., Stark, M. R., Keenan, R. J., Myall, D. J., MacAskill, M. R., Pitcher, T. L., et al. (2019). Beta Amyloid Deposition Is Not Associated With Cognitive Impairment in Parkinson's Disease. Frontiers in neurology. https://doi.org/10.3389/fneur.2019.00391
Vancouver
Melzer TR, Stark MR, Keenan RJ, Myall DJ, MacAskill MR, Pitcher TL, et al. Beta Amyloid Deposition Is Not Associated With Cognitive Impairment in Parkinson's Disease. Frontiers in neurology. 2019. doi:10.3389/fneur.2019.00391. PMID: 31105633.
BibTeX
@article{melzer2019-31105633,
author = {Melzer, T. R. and Stark, M. R. and Keenan, R. J. and Myall, D. J. and MacAskill, M. R. and Pitcher, T. L. and Livingston, L. and Grenfell, S. and others},
title = {{Beta Amyloid Deposition Is Not Associated With Cognitive Impairment in Parkinson's Disease}},
journal = {Frontiers in neurology},
year = {2019},
doi = {10.3389/fneur.2019.00391},
pmid = {31105633},
url = {https://doi.org/10.3389/fneur.2019.00391}
}
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