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CSF proteins and resting-state functional connectivity in Parkinson disease
Meghan C Campbell, Jonathan M Koller, Abraham Z Snyder, Chandana Buddhala, Paul T Kotzbauer, Joel S Perlmutter. Neurology, 2015-05-15
Topic: Brain imaging, connectivity and assessment
Participants with PD had significantly reduced sensorimotor functional connectivity, which correlated with reduced CSF levels of α-synuclein. The PD group also had significantly stronger default mode network functional connectivity that did not correlate with CSF β-amyloid (Aβ)42 or PiB uptake. In contrast, default mode network functional connectivity in the control group did correlate with CSF Aβ42 levels. Functional connectivity was similar between groups in the dorsal attention, control, and salience networks. These results suggest that abnormal α-synuclein accumulation, but not Aβ, contributes to the disruption of motor-related functional connectivity in PD. Furthermore, correlating CSF protein measures with the strength of resting-state networks provides a direct link between abnormal α-synuclein metabolism and disrupted brain function in PD.
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APA 7th
Campbell, M. C., Koller, J. M., Snyder, A. Z., Buddhala, C., Kotzbauer, P. T., & Perlmutter, J. S. (2015). CSF proteins and resting-state functional connectivity in Parkinson disease. Neurology. https://doi.org/10.1212/wnl.0000000000001681
Vancouver
Campbell MC, Koller JM, Snyder AZ, Buddhala C, Kotzbauer PT, Perlmutter JS. CSF proteins and resting-state functional connectivity in Parkinson disease. Neurology. 2015. doi:10.1212/wnl.0000000000001681. PMID: 25979701.
BibTeX
@article{campbell2015-25979701,
author = {Campbell, Meghan C and Koller, Jonathan M and Snyder, Abraham Z and Buddhala, Chandana and Kotzbauer, Paul T and Perlmutter, Joel S},
title = {{CSF proteins and resting-state functional connectivity in Parkinson disease}},
journal = {Neurology},
year = {2015},
doi = {10.1212/wnl.0000000000001681},
pmid = {25979701},
url = {https://doi.org/10.1212/wnl.0000000000001681}
}
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Key findings
- Participants with PD had significantly reduced sensorimotor functional connectivity, which correlated with reduced CSF levels of α-synuclein.
- The PD group also had significantly stronger default mode network functional connectivity that did not correlate with CSF β-amyloid (Aβ)42 or PiB uptake.
- In contrast, default mode network functional connectivity in the control group did correlate with CSF Aβ42 levels.
- Functional connectivity was similar between groups in the dorsal attention, control, and salience networks.
- These results suggest that abnormal α-synuclein accumulation, but not Aβ, contributes to the disruption of motor-related functional connectivity in PD.
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Study details
- Participants43
- Evidence strengthLow
How this study scored 48/100
Published in a leading specialty journal. Scored zero for study design, effect reported and randomised / blinded because the record does not state it. We have no data on journal's citation record, times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record, multi-centre collaboration and free to read, so those were left out: it earned 27 of the 56 points we could judge it on, which is 48 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 9 / 10 | Tier 2 — leading specialty journal (Neurology) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| 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 | 2015 — within 20 year(s) of the newest study here |
| Sample size | 1 / 4 | 43 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 | — / 7 | No citation count (not found in OpenAlex) — left out of this score |
| Citations per year | — / 5 | No citation count or no year — left out of this score |
| Impact for its field and year | — / 6 | No field-weighted citation impact (OpenAlex has none yet) — left out of this score |
| Cited by studies here | — / 6 | Not yet checked against this library's citation graph — left out of this score |
| Still being cited | — / 4 | No yearly citation counts — left out of this score |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | — / 3 | No institution listed in OpenAlex — left out of this score |
| Multi-centre collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 25979701) |
| Free to read | — / 2 | Access not recorded — left out of this score |
| Points | 27 / 56 | Scored on 10 of 20 parts. We have no data for the rest, so they are left out: 27 of the 56 points we could judge it on is 48 out of 100. |
| Total | 48 / 100 | — |
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