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36/100

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Brain scans and imaging

Topic: Gut, metabolism and diet

Plain-language summary

Purpose of review To summarize recent findings that docosahexaenoate (DHA) is the precursor of stereospecific derivatives with anti-inflammatory and cytoprotective properties. Recent findings The docosahexaenoate-derived mediator neuroprotectin D1 is formed in retinal pigment epithelial cells when confronted with oxidative stress, in the brain during experimental stroke, and in the human brain from Alzheimer's disease patients as well as in human brain cells in culture. Neuroprotectin D1 displays potent anti-inflammatory and neuroprotective bioactivity. Summary Here, we summarize recent studies demonstrating that in brain ischemia-reperfusion and in retinal pigment epithelial cells exposed to oxidative stress stereospecific docosahexaenoate-oxygenation pathways are activated and lead to the formation of docosanoid messengers. Two docosahexaenoate-oxygenation pathways were identified: the first is responsible for the formation of the messenger neuroprotectin D1 and the second pathway, which is active in the presence of aspirin, leads to the formation of the resolvin-type mediators (17R-DHA). Neuroprotectin D1 induces antiapoptotic, anti-inflammatory signaling and is neuroprotective.

Cite this study APA, Vancouver, BibTeX · download .bib or .ris

APA 7th

Bazan, N. G. (2007). Omega-3 fatty acids, pro-inflammatory signaling and neuroprotection. Current opinion in clinical nutrition and metabolic care. https://doi.org/10.1097/mco.0b013e32802b7030

Vancouver

Bazan NG. Omega-3 fatty acids, pro-inflammatory signaling and neuroprotection. Current opinion in clinical nutrition and metabolic care. 2007. doi:10.1097/mco.0b013e32802b7030. PMID: 17285000.

BibTeX

@article{bazan2007-17285000,
  author  = {Bazan, N. G.},
  title   = {{Omega-3 fatty acids, pro-inflammatory signaling and neuroprotection}},
  journal = {Current opinion in clinical nutrition and metabolic care},
  year    = {2007},
  doi     = {10.1097/mco.0b013e32802b7030},
  pmid    = {17285000},
  url     = {https://doi.org/10.1097/mco.0b013e32802b7030}
}

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How to read this study

Design: this is a narrative review. It summarises a field without a fixed search method, so it shows how authors read the evidence rather than measuring it. Use it to find the primary studies, not as a result in itself.
Size: the record gives no participant count. Look for one in the original before trusting a pattern.
Effect: the record gives no effect size, so the summary above cannot say how large any difference was.

What the evidence grade means here

This page is graded low. alzhub.org assigns the grade automatically from keywords in the abstract, not from reading the paper. Low means the abstract matched neither pattern. It is the default label, and it does not mean the work is poor; many sound lab and imaging papers land here. It can add at most 5 of the 100 points in the study score, and it is a label about design, not a verdict on whether the findings are true.

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Key findings

Recent findings The docosahexaenoate-derived mediator neuroprotectin D1 is formed in retinal pigment epithelial cells when confronted with oxidative stress, in the brain during experimental stroke, and in the human brain from Alzheimer's disease patients as well as in human brain cells in culture.
Neuroprotectin D1 displays potent anti-inflammatory and neuroprotective bioactivity.
Summary Here, we summarize recent studies demonstrating that in brain ischemia-reperfusion and in retinal pigment epithelial cells exposed to oxidative stress stereospecific docosahexaenoate-oxygenation pathways are activated and lead to the formation of docosanoid messengers.
Two docosahexaenoate-oxygenation pathways were identified: the first is responsible for the formation of the messenger neuroprotectin D1 and the second pathway, which is active in the presence of aspirin, leads to the formation of the resolvin-type mediators (17R-DHA).
Neuroprotectin D1 induces antiapoptotic, anti-inflammatory signaling and is neuroprotective.

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Study details

Evidence strengthLow

How this study scored 36/100

Published in a peer-reviewed journal. Scored zero for study design, 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 21 of the 58 points we could judge it on, which is 36 out of 100.

Component	Points	Why
Journal tier	7 / 10	Tier 3 — peer-reviewed journal (Current opinion in clinical nutrition and metabolic care)
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	2007 — 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)
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 17285000)
Free to read	0 / 2	Behind a paywall — scores zero
Points	21 / 58	Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 21 of the 58 points we could judge it on is 36 out of 100.
Total	36 / 100	—

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