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Brain injury-induced dysfunction of the blood brain barrier as a risk for dementia
Abrahamson EE, Ikonomovic MD.. Experimental neurology, 2020-02-21
Topic: Risk, prevention and care in population studies
The blood-brain barrier (BBB) is a complex and dynamic physiological interface between brain parenchyma and cerebral vasculature. It is composed of closely interacting cells and signaling molecules that regulate movement of solutes, ions, nutrients, macromolecules, and immune cells into the brain and removal of products of normal and abnormal brain cell metabolism. Dysfunction of multiple components of the BBB occurs in aging, inflammatory diseases, traumatic brain injury (TBI, severe or mild repetitive), and in chronic degenerative dementing disorders for which aging, inflammation, and TBI are considered risk factors. BBB permeability changes after TBI result in leakage of serum proteins, influx of immune cells, perivascular inflammation, as well as impairment of efflux transporter systems and accumulation of aggregation-prone molecules involved in hallmark pathologies of neurodegenerative diseases with dementia. In addition, cerebral vascular dysfunction with persistent alterations in cerebral blood flow and neurovascular coupling contribute to brain ischemia, neuronal degeneration, and synaptic dysfunction. While the idea of TBI as a risk factor for dementia is supported by many shared pathological features, it remains a hypothesis that needs further testing in experimental models and in human studies. The current review focusses on pathological mechanisms shared between TBI and neurodegenerative disorders characterized by accumulation of pathological protein aggregates, such as Alzheimer's disease and chronic traumatic encephalopathy. We discuss critical knowledge gaps in the field that need to be explored to clarify the relationship between TBI and risk for dementia and emphasize the need for longitudinal in vivo studies using imaging and biomarkers of BBB dysfunction in people with single or multiple TBI.
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APA 7th
Abrahamson, E. E., & Ikonomovic, M. D. (2020). Brain injury-induced dysfunction of the blood brain barrier as a risk for dementia. Experimental neurology. https://doi.org/10.1016/j.expneurol.2020.113257
Vancouver
Abrahamson EE, Ikonomovic MD. Brain injury-induced dysfunction of the blood brain barrier as a risk for dementia. Experimental neurology. 2020. doi:10.1016/j.expneurol.2020.113257. PMID: 32092298.
BibTeX
@article{abrahamson2020-32092298,
author = {Abrahamson, E. E. and Ikonomovic, M. D.},
title = {{Brain injury-induced dysfunction of the blood brain barrier as a risk for dementia}},
journal = {Experimental neurology},
year = {2020},
doi = {10.1016/j.expneurol.2020.113257},
pmid = {32092298},
url = {https://doi.org/10.1016/j.expneurol.2020.113257}
}
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Key findings
- BBB permeability changes after TBI result in leakage of serum proteins, influx of immune cells, perivascular inflammation, as well as impairment of efflux transporter systems and accumulation of aggregation-prone molecules involved in hallmark pathologies of neurodegenerative diseases with dementia.
Study details
- Study designlongitudinal study
- Evidence strengthModerate
How this study scored 53/100
Published in a peer-reviewed journal, and it is a longitudinal study following the same people over time. Scored zero for sample size, effect reported, studied in people and randomized / 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 and multicenter collaboration, so those were left out: it earned 31 of the 58 points we could judge it on, which is 53 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Experimental neurology) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| Study design | 7 / 12 | A longitudinal study following the same people over time |
| Strength of evidence | 3 / 5 | Rated “moderate” 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 | 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) |
| Randomized / blinded | 0 / 2 | No randomization 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 |
| Multicenter collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 32092298) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Points | 31 / 58 | Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 31 of the 58 points we could judge it on is 53 out of 100. |
| Total | 53 / 100 | — |
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