Evidence map›Paper›PMID 36373322›Full record

ArticleJournal of Alzheimer's disease : JAD2023

Polyunsaturated Fatty Acids Mend Macrophage Transcriptome, Glycome, and Phenotype in the Patients with Neurodegenerative Diseases, Including Alzheimer's Disease.

Mary Dover, Taylor Moseley, Adrienne Biskaduros, Mousumi Paulchakrabarti, Sung Hee Hwang, Bruce Hammock, Biswa Choudhury, Karolina Elżbieta Kaczor-Urbanowicz, Andrzej Urbanowicz, Marco Morselli and 5 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of Alzheimer's disease : JAD, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

4 citing papers in PubMed, 7 citations in OpenAlex.

  1. Tuft Cells in the Gut Limit Cognitive Disorders by Regulating Gut Homeostasis.Cellular and molecular gastroenterology and hepatology · 2026
    Article
  2. Review
  3. Article
  4. Review
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

15 authors at 5 institutions in 2 countries.

Mary DoverDepartment of Molecular, Cell and Developmental Biology, UCLA School of Life Sciences, Los Angeles, CA, USA.
Taylor MoseleyDepartment of Molecular, Cell and Developmental Biology, UCLA School of Life Sciences, Los Angeles, CA, USA.
Adrienne BiskadurosDepartment of Molecular, Cell and Developmental Biology, UCLA School of Life Sciences, Los Angeles, CA, USA.
Mousumi PaulchakrabartiGlycoAnalytics Core, University of California SanDiego Health Sciences, La Jolla, CA, USA.
Sung Hee HwangDepartment of Entomology and Nematology, and UCDavis Comprehensive Cancer Center, University of California - Davis, Davis, CA, USA.
Bruce HammockDepartment of Entomology and Nematology, and UCDavis Comprehensive Cancer Center, University of California - Davis, Davis, CA, USA.
Biswa ChoudhuryGlycoAnalytics Core, University of California SanDiego Health Sciences, La Jolla, CA, USA.
Karolina Elżbieta Kaczor-UrbanowiczUCLA Institute for Quantitative and Computational Biosciences, UCLA, Los Angeles, CA, USA.
Andrzej UrbanowiczInstitute of Control and Computation Engineering, Warsaw University of Technology, Warsaw, Poland.
Marco MorselliDepartment of Molecular, Cell and Developmental Biology, UCLA School of Life Sciences, Los Angeles, CA, USA.
Johnny DangDepartment of Molecular, Cell and Developmental Biology, UCLA School of Life Sciences, Los Angeles, CA, USA.
Matteo PellegriniDepartment of Molecular, Cell and Developmental Biology, UCLA School of Life Sciences, Los Angeles, CA, USA.
Ketema PaulDepartment of Integrated Biology and Physiology, UCLA School of Life Sciences, Los Angeles, CA, USA.
Laurent A BentolilaAdvanced Light Microscopy and Spectroscopy Laboratory, California Nano Systems Institute, UCLA, Los Angeles, CA, USA.
Milan FialaDepartment of Molecular, Cell and Developmental Biology, UCLA School of Life Sciences, Los Angeles, CA, USA.
University of California, Los Angeles · USUC Davis Comprehensive Cancer CenterUniversity of California San Diego · USCalifornia NanoSystems Institute · USWarsaw University of Technology · PL

Funding

Workshop on Environmental Technology Transfer and EntrepreneurshipP42ES004699 · NIEHS · UNIVERSITY OF CALIFORNIA DAVIS · PI HAMMOCK, BRUCE D · 1987 to 2021
$50.1M
Supplement for bioactive lipids as effectors and indicators of the deleterious effects of human healthR35ES030443 · NIEHS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI MORISSEAU, CHRISTOPHE HP · 2019 to 2025
$5.8M
The impact of sex chromosomes on the ability to recover from sleep lossR01NS078410 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI PAUL, KETEMA N · 2012 to 2025
$3.7M
NIEHS NIH HHS P42 ES004699NIEHS NIH HHS R35 ES030443NINDS NIH HHS R01 NS078410
6 · The paper itself

Abstract

backgroundMacrophages of healthy subjects have a pro-resolution phenotype, upload amyloid-β (Aβ) into endosomes, and degrade Aβ, whereas macrophages of patients with Alzheimer's disease (AD) generally have a pro-inflammatory phenotype and lack energy for brain clearance of Aβ.

objectiveTo clarify the pathogenesis of sporadic AD and therapeutic effects of polyunsaturated fatty acids (PUFA) with vitamins B and D and antioxidants on monocyte/macrophage (MM) migration in the AD brain, MM transcripts in energy and Aβ degradation, MM glycome, and macrophage clearance of Aβ.

methodsWe followed for 31.3 months (mean) ten PUFA-supplemented neurodegenerative patients: 3 with subjective cognitive impairment (SCI), 2 with mild cognitive impairment (MCI), 3 MCI/vascular cognitive impairment, 2 with dementia with Lewy bodies, and 7 non-supplemented caregivers. We examined: monocyte migration in the brain and a blood-brain barrier model by immunochemistry and electron microscopy; macrophage transcriptome by RNAseq; macrophage glycome by N-glycan profiling and LTQ-Orbitrap mass spectrometry; and macrophage phenotype and phagocytosis by immunofluorescence.

resultsMM invade Aβ plaques, upload but do not degrade Aβ, and release Aβ into vessels, which develop cerebrovascular amyloid angiopathy (CAA); PUFA upregulate energy and Aβ degradation enzyme transcripts in macrophages; PUFA enhance sialylated N-glycans in macrophages; PUFA reduce oxidative stress and increase pro-resolution MM phenotype, mitochondrial membrane potential, and Aβ phagocytosis (p < 0.001).

conclusionMacrophages of SCI, MCI, and AD patients have interrelated defects in the transcriptome, glycome, Aβ phagocytosis, and Aβ degradation. PUFA mend macrophage transcriptome, enrich glycome, enhance Aβ clearance, and benefit the cognition of early-stage AD patients.

Indexed as

Alzheimer DiseaseNeurodegenerative DiseasesAmyloid beta-PeptidesBrainFatty Acids, UnsaturatedHumansMacrophagesPhenotypeTranscriptomeAmyloid beta-PeptidesFatty Acids, UnsaturatedAlzheimer’s diseaseamyloid-βcerebrovascular amyloid angiopathycoenzyme Q2glycomemacrophagemitochondrial membrane potentialphagocytosispolyunsaturated fatty acidstranscriptome

Identifiers

PMID36373322
PMCPMC9881025
OpenAlexW4308512206

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.