Evidence map›Paper›PMID 26369878›Full record

ArticleNeurobiology of disease2015

Dietary DHA supplementation in an APP/PS1 transgenic rat model of AD reduces behavioral and Aβ pathology and modulates Aβ oligomerization.

Edmond Teng, Karen Taylor, Tina Bilousova, David Weiland, Thaidan Pham, Xiaohong Zuo, Fusheng Yang, Ping-Ping Chen, Charles G Glabe, Alison Takacs and 3 more

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

Article in Neurobiology of disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
5.6field-weighted citation impact, top 4% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.

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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

13 authors at 6 institutions in 3 countries.

Edmond TengDepartment of Neurology, David Geffen School of Medicine, University of California, Los Angeles, CA, USA; Veterans Affairs Greater Los Angeles Healthcare System, Los Angeles, CA, USA. Electronic address: eteng@ucla.edu.
Karen TaylorDepartment of Neurology, David Geffen School of Medicine, University of California, Los Angeles, CA, USA.
Tina BilousovaDepartment of Neurology, David Geffen School of Medicine, University of California, Los Angeles, CA, USA.
David WeilandDepartment of Neurology, David Geffen School of Medicine, University of California, Los Angeles, CA, USA; Veterans Affairs Greater Los Angeles Healthcare System, Los Angeles, CA, USA.
Thaidan PhamDepartment of Neurology, David Geffen School of Medicine, University of California, Los Angeles, CA, USA.
Xiaohong ZuoDepartment of Neurology, David Geffen School of Medicine, University of California, Los Angeles, CA, USA; Veterans Affairs Greater Los Angeles Healthcare System, Los Angeles, CA, USA; Department of Neurobiology and Neurology, Beijing Institute of Geriatrics, Xuanwu Hospital, Capital Medical University, Beijing, China.
Fusheng YangDepartment of Neurology, David Geffen School of Medicine, University of California, Los Angeles, CA, USA; Veterans Affairs Greater Los Angeles Healthcare System, Los Angeles, CA, USA.
Ping-Ping ChenDepartment of Neurology, David Geffen School of Medicine, University of California, Los Angeles, CA, USA; Veterans Affairs Greater Los Angeles Healthcare System, Los Angeles, CA, USA.
Charles G GlabeDepartment of Molecular Biology and Biochemistry, University of California, Irvine, CA, USA; Biochemistry Department and Experimental Biochemistry Unit, King Fahd Medical Research Center, King Abdulaziz University, Jeddah, Saudi Arabia.
Alison TakacsRetina Foundation of the Southwest, Dallas, TX, USA.
Dennis R HoffmanRetina Foundation of the Southwest, Dallas, TX, USA; Department of Ophthalmology, UT Southwestern Medical Center, Dallas, TX, USA.
Sally A FrautschyDepartment of Neurology, David Geffen School of Medicine, University of California, Los Angeles, CA, USA; Veterans Affairs Greater Los Angeles Healthcare System, Los Angeles, CA, USA.
Gregory M ColeDepartment of Neurology, David Geffen School of Medicine, University of California, Los Angeles, CA, USA; Veterans Affairs Greater Los Angeles Healthcare System, Los Angeles, CA, USA.
VA Greater Los Angeles Healthcare System · USUniversity of California, Los Angeles · USCapital Medical University · CNKing Abdulaziz University · SARetina Foundation of the Southwest · USSouthwestern Medical Center · US

Funding

TISSUE REPOSITORY COREP01AG000538 · NIA · UNIVERSITY OF CALIFORNIA-IRVINE · PI COTMAN, CARL WAYNE · 1985 to 2018
$24.8M
Diet and Exercise (DE) Program for Alzheimer PreventionRC1AG035878 · NIA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI COLE, GREGORY M, FRAUTSCHY, SALLY ANN · 2009 to 2010
$1.0M
Assessment of Biomarkers and Behavior in a Transgenic Rat Model of ADK08AG034628 · NIA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI TENG, EDMOND HUATUNG · 2009 to 2013
$540k
How to modulate innate immune function to prevent age-related neurodegenerationI01BX002476 · VA · VA GREATER LOS ANGELES HEALTHCARE SYSTEM · PI COLE, GREGORY M · 2015 to 2018
–
BLRD VA I01 BX002476NIA NIH HHS K08 AG034628NIA NIH HHS K08 AG34628NIA NIH HHS P01 AG000538NIA NIH HHS RC1 AG035878
6 · The paper itself

Abstract

Increased dietary consumption of docosahexaenoic acid (DHA) is associated with decreased risk for Alzheimer's disease (AD). These effects have been postulated to arise from DHA's pleiotropic effects on AD pathophysiology, including its effects on β-amyloid (Aβ) production, aggregation, and toxicity. While in vitro studies suggest that DHA may inhibit and reverse the formation of toxic Aβ oligomers, it remains uncertain whether these mechanisms operate in vivo at the physiological concentrations of DHA attainable through dietary supplementation. We sought to clarify the effects of dietary DHA supplementation on Aβ indices in a transgenic APP/PS1 rat model of AD. Animals maintained on a DHA-supplemented diet exhibited reductions in hippocampal Aβ plaque density and modest improvements on behavioral testing relative to those maintained on a DHA-depleted diet. However, DHA supplementation also increased overall soluble Aβ oligomer levels in the hippocampus. Further quantification of specific conformational populations of Aβ oligomers indicated that DHA supplementation increased fibrillar (i.e. putatively less toxic) Aβ oligomers and decreased prefibrillar (i.e. putatively more toxic) Aβ oligomers. These results provide in vivo evidence suggesting that DHA can modulate Aβ aggregation by stabilizing soluble fibrillar Aβ oligomers and thus reduce the formation of both Aβ plaques and prefibrillar Aβ oligomers. However, since fibrillar Aβ oligomers still retain inherent neurotoxicity, DHA may need to be combined with other interventions that can additionally reduce fibrillar Aβ oligomer levels for more effective prevention of AD in clinical settings.

Indexed as

Dietary SupplementsDocosahexaenoic AcidsAlzheimer DiseaseAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsDisease Models, AnimalFemaleHippocampusHumansMaleMaze LearningPeptide FragmentsPlaque, AmyloidPresenilin-1Protein MultimerizationAmyloid beta-Peptidesamyloid beta-protein (1-42)Amyloid beta-Protein PrecursorAPP protein, humanDocosahexaenoic AcidsPeptide FragmentsPresenilin-1PSEN1 protein, humanAggregationAlzheimer's diseaseDocosahexaenoic acidFibrillarHippocampusOligomersPrefibrillarTransgenicβ-amyloid

Identifiers

PMID26369878
PMCPMC4641021
OpenAlexW1624443988

What OpenQuestion holds

Textmetadata
LicenceTDM
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.