Evidence map›Paper›PMID 22978403›Full record

ArticleLipids in health and disease2012

Restoration of dietary-fat induced blood-brain barrier dysfunction by anti-inflammatory lipid-modulating agents.

Menuka Pallebage-Gamarallage, Virginie Lam, Ryusuke Takechi, Susan Galloway, Karin Clark, John Mamo

Open access · goldAbstract read
In one paragraph

Article in Lipids in health and disease, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.8field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

27 citing papers in PubMed, 55 citations in OpenAlex.

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  14. Common neurodegenerative pathways in obesity, diabetes, and Alzheimer's disease.Biochimica et biophysica acta. Molecular basis of disease · 2017
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Menuka Pallebage-GamarallageSchool of Public Health, Curtin University, Kent Street, Bentley, 6102, Western Australia. J.Mamo@curtin.edu.au
Virginie Lam
Ryusuke Takechi
Susan Galloway
Karin Clark
John Mamo
Curtin University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSeveral studies have identified use of non-steroidal-anti-inflammatory drugs and statins for prevention of dementia, but their efficacy in slowing progression is not well understood. Cerebrovascular disturbances are common pathological feature of Alzheimer's disease. We previously reported chronic ingestion of saturated fatty acids (SFA) compromises blood-brain barrier (BBB) integrity resulting in cerebral extravasation of plasma proteins and inflammation. However, the SFA-induced parenchymal accumulation of plasma proteins could be prevented by co-administration of some cholesterol lowering agents. Restoration of BBB dysfunction is clinically relevant, so the purpose of this study was to explore lipid-lowering agents could reverse BBB disturbances induced by chronic ingestion of SFA's.

methodsWild-type mice were fed an SFA diet for 12 weeks to induce BBB dysfunction, and then randomised to receive atorvastatin, pravastatin or ibuprofen in combination with the SFA-rich diet for 2 or 8 weeks. Abundance of plasma-derived immunoglobulin-G (IgG) and amyloid-β enriched apolipoprotein (apo)-B lipoproteins within brain parenchyme were quantified utilising immunofluorescence microscopy.

resultsAtorvastatin treatment for 2 and 8 weeks restored BBB integrity, indicated by a substantial reduction of IgG and apo B, particularly within the hippocampus. Pravastatin, a water-soluble statin was less effective than atorvastatin (lipid-soluble). Statin effects were independent of changes in plasma lipid homeostasis. Ibuprofen, a lipid-soluble cyclooxygenase inhibitor attenuated cerebral accumulation of IgG and apo B as effectively as atorvastatin. Our findings are consistent with the drug effects being independent of plasma lipid homeostasis.

conclusionOur findings suggest that BBB dysfunction induced by chronic ingestion of SFA is reversible with timely introduction and sustained treatment with agents that suppress inflammation.

Indexed as

Amyloid beta-PeptidesAnimalsAnti-Inflammatory Agents, Non-SteroidalApolipoproteins BAtorvastatinBlood-Brain BarrierBrainDiet, High-FatFemaleHeptanoic AcidsHydroxymethylglutaryl-CoA Reductase InhibitorsHypolipidemic AgentsIbuprofenImmunoglobulin GMiceMice, Inbred C57BLAmyloid beta-PeptidesAnti-Inflammatory Agents, Non-SteroidalApolipoproteins BAtorvastatinHeptanoic AcidsHydroxymethylglutaryl-CoA Reductase InhibitorsHypolipidemic AgentsIbuprofenImmunoglobulin GPravastatinPyrroles

Identifiers

PMID22978403
PMCPMC3492058
OpenAlexW1999652136

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.