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Downregulation of synapse-associated protein expression and loss of homeostatic microglial control in cerebrospinal fluid of infectious patients with delirium and patients with Alzheimer's disease
Peters van Ton AM, Verbeek MM, Alkema W, Pickkers P, Abdo WF.. Brain, behavior, and immunity, 2020-06-24
Topic: Brain proteins, microglia and lab models
Delirium is a complex and multifactorial condition associated with long-term cognitive decline. Due to the strong links between systemic inflammation, delirium and dementia we hypothesized that responses within the brain in patients who develop delirium could show biochemical overlap with patients with Alzheimer's disease (AD). In this observational study we analyzed protein expression signatures in cerebrospinal fluid (CSF) from 15 patients with infectious delirium and compared these to 29 patients with AD, 30 infectious patients without delirium and 15 non-infectious controls free of neurological disease. A proximity extension assay was performed measuring a total of 184 inflammatory and neurology-related proteins. Eight inflammatory proteins (4%), including the key neuron-microglia communication marker CX3CL1 (fractalkine), were significantly upregulated in both delirium and AD, compared to infectious patients without delirium. Likewise, 23 proteins (13%) showed downregulation in both delirium and AD, relative to infectious patients without delirium, which interestingly included CD200R1, another neuron-microglia communication marker, as well as a cluster of proteins related to synapse formation and function. Synaptopathy is an early event in AD and correlates strongly with cognitive dysfunction. These results were partially mediated by aging, which is an important predisposing risk factor among many others for both conditions. Within this study we report the first in vivo human evidence suggesting that synapse pathology and loss of homeostatic microglial control is involved in the pathophysiology of both infectious delirium and AD and thus may provide a link for the association between infections, delirium and long-term cognitive decline.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Peters van Ton, A. M., Verbeek, M. M., Alkema, W., Pickkers, P., & Abdo, W. F. (2020). Downregulation of synapse-associated protein expression and loss of homeostatic microglial control in cerebrospinal fluid of infectious patients with delirium and patients with Alzheimer's disease. Brain, behavior, and immunity. https://doi.org/10.1016/j.bbi.2020.06.027
Vancouver
Peters van Ton AM, Verbeek MM, Alkema W, Pickkers P, Abdo WF. Downregulation of synapse-associated protein expression and loss of homeostatic microglial control in cerebrospinal fluid of infectious patients with delirium and patients with Alzheimer's disease. Brain, behavior, and immunity. 2020. doi:10.1016/j.bbi.2020.06.027. PMID: 32592865.
BibTeX
@article{petersvanton2020-32592865,
author = {Peters van Ton, A. M. and Verbeek, M. M. and Alkema, W. and Pickkers, P. and Abdo, W. F.},
title = {{Downregulation of synapse-associated protein expression and loss of homeostatic microglial control in cerebrospinal fluid of infectious patients with delirium and patients with Alzheimer's disease}},
journal = {Brain, behavior, and immunity},
year = {2020},
doi = {10.1016/j.bbi.2020.06.027},
pmid = {32592865},
url = {https://doi.org/10.1016/j.bbi.2020.06.027}
}
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.
Key findings
- Delirium is a complex and multifactorial condition associated with long-term cognitive decline.
- Eight inflammatory proteins (4%), including the key neuron-microglia communication marker CX3CL1 (fractalkine), were significantly upregulated in both delirium and AD, compared to infectious patients without delirium.
- These results were partially mediated by aging, which is an important predisposing risk factor among many others for both conditions.
- Within this study we report the first in vivo human evidence suggesting that synapse pathology and loss of homeostatic microglial control is involved in the pathophysiology of both infectious delirium and AD and thus may provide a link for the association between infections, delirium and long-term cognitive decline.
Why it matters
Comparing cerebrospinal fluid from 15 patients with infection-related delirium, 29 with Alzheimer's disease and other comparison groups, researchers found 8 inflammatory proteins raised and 23 proteins lowered in both delirium and Alzheimer's. These included CX3CL1 and CD200R1, markers of communication between neurons and microglia (the brain's immune cells), and proteins involved in synapses. The authors suggest synapse damage and loss of microglial control may be shared by both conditions, possibly linking infections, delirium and long-term cognitive decline.
Study details
- Participants15
- Evidence strengthLow
How this study scored 44/100
Published in a peer-reviewed journal. Scored zero for study design, effect reported and randomized / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Brain, behavior, and immunity) |
| Journal's citation record | 2 / 4 | Brain Behavior and Immunity: journal h-index 249 (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 | 2 / 5 | 2020 — within 10 year(s) of the newest study here |
| Sample size | 1 / 4 | 15 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) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 4 / 7 | Cited 46 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 5.8 citations a year over 8 year(s) since 2020 |
| Impact for its field and year | 2 / 6 | Cited 1.8× 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 24 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Wilson Farid Abdo: h-index 28 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | Radboud University Nijmegen: institution h-index 1,143 (OpenAlex) |
| Multicenter collaboration | 2 / 3 | OpenAlex lists 4 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 32592865) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 44 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1016/j.bbi.2020.06.027
- PubMed: 32592865
- Original source →
- Free full text: Brain Behavior and Immunity →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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