Evidence map›Paper›PMID 36841786›Full record

ReviewGenes & nutrition2023

Peripheral metabolism of lipoprotein-amyloid beta as a risk factor for Alzheimer's disease: potential interactive effects of APOE genotype with dietary fats.

Zachary J D'Alonzo, Virginie Lam, Ryu Takechi, Michael Nesbit, Mauro Vaccarezza, John C L Mamo

Open access · goldAbstract readReview
In one paragraph

Review in Genes & nutrition, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

10 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
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  9. Article
  10. Oxysterols in Central and Peripheral Synaptic Communication.Advances in experimental medicine and biology · 2024
    Article
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.

Zachary J D'AlonzoFaculty of Health Sciences, Curtin Medical School, Curtin University, Perth, Western Australia, Australia.
Virginie LamFaculty of Health Sciences, Curtin Health Innovation Research Institute, Curtin University, Perth, Western Australia, Australia.
Ryu TakechiFaculty of Health Sciences, Curtin Health Innovation Research Institute, Curtin University, Perth, Western Australia, Australia.
Michael NesbitFaculty of Health Sciences, Curtin Health Innovation Research Institute, Curtin University, Perth, Western Australia, Australia.
Mauro VaccarezzaFaculty of Health Sciences, Curtin Medical School, Curtin University, Perth, Western Australia, Australia.
John C L MamoFaculty of Health Sciences, Curtin Health Innovation Research Institute, Curtin University, Perth, Western Australia, Australia. j.mamo@curtin.edu.au.
Curtin University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disorder pathologically characterized by brain parenchymal abundance of amyloid-beta (Aβ) and the accumulation of lipofuscin material that is rich in neutral lipids. However, the mechanisms for aetiology of AD are presently not established. There is increasing evidence that metabolism of lipoprotein-Aβ in blood is associated with AD risk, via a microvascular axis that features breakdown of the blood-brain barrier, extravasation of lipoprotein-Aβ to brain parenchyme and thereafter heightened inflammation. A peripheral lipoprotein-Aβ/capillary axis for AD reconciles alternate hypotheses for a vascular, or amyloid origin of disease, with amyloidosis being probably consequential. Dietary fats may markedly influence the plasma abundance of lipoprotein-Aβ and by extension AD risk. Similarly, apolipoprotein E (Apo E) serves as the primary ligand by which lipoproteins are cleared from plasma via high-affinity receptors, for binding to extracellular matrices and thereafter for uptake of lipoprotein-Aβ via resident inflammatory cells. The epsilon APOE ε4 isoform, a major risk factor for AD, is associated with delayed catabolism of lipoproteins and by extension may increase AD risk due to increased exposure to circulating lipoprotein-Aβ and microvascular corruption.

Indexed as

Alzheimer’s diseaseAmyloid-betaAPOEDementiaGeneticLipoproteinNutritionSaturated fatVascular

Identifiers

PMID36841786
PMCPMC9960179
OpenAlexW4321850178

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.