Evidence map›Paper›PMID 32190891›Full record

ArticleAdvances in nutrition (Bethesda, Md.)2020

Perspective: The Potential Role of Circulating Lysophosphatidylcholine in Neuroprotection against Alzheimer Disease.

Richard D Semba

Open access · bronzeAbstract read
In one paragraph

Article in Advances in nutrition (Bethesda, Md.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

47 citing papers in PubMed, 74 citations in OpenAlex.

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  16. Extracellular Vesicle Lipids and Their Role in Delivery.Journal of extracellular biology · 2025
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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

1 author at 1 institution in 1 country.

Richard D SembaWilmer Eye Institute, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Johns Hopkins University · US

Funding

Oxidative stress and the pathogenesis of sarcopenia and disability in older womenR01AG027012 · NIA · JOHNS HOPKINS UNIVERSITY · PI SEMBA, RICHARD D · 2005 to 2018
$3.6M
Systemic rejuvenating factors and human aging phenotypes.R01AG057723 · NIA · JOHNS HOPKINS UNIVERSITY · PI SEMBA, RICHARD D · 2018 to 2022
$1.8M
Lysophosphatidylcholines and Cognition (L-COG) StudyR21HL153471 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI SEMBA, RICHARD D · 2020 to 2021
$246k
NHLBI NIH HHS R21 HL153471NIA NIH HHS R01 AG027012NIA NIH HHS R01 AG057723
6 · The paper itself

Abstract

Alzheimer disease (AD), the most common cause of dementia, is a progressive disorder involving cognitive impairment, loss of learning and memory, and neurodegeneration affecting wide areas of the cerebral cortex and hippocampus. AD is characterized by altered lipid metabolism in the brain. Lower concentrations of long-chain PUFAs have been described in the frontal cortex, entorhinal cortex, and hippocampus in the brain in AD. The brain can synthesize only a few fatty acids; thus, most fatty acids must enter the brain from the blood. Recent studies show that PUFAs such as DHA (22:6) are transported across the blood-brain barrier (BBB) in the form of lysophosphatidylcholine (LPC) via a specific LPC receptor at the BBB known as the sodium-dependent LPC symporter 1 (MFSD2A). Higher dietary PUFA intake is associated with decreased risk of cognitive decline and dementia in observational studies; however, PUFA supplementation, with fatty acids esterified in triacylglycerols did not prevent cognitive decline in clinical trials. Recent studies show that LPC is the preferred carrier of PUFAs across the BBB into the brain. An insufficient pool of circulating LPC containing long-chain fatty acids could potentially limit the supply of long-chain fatty acids to the brain, including PUFAs such as DHA, and play a role in the pathobiology of AD. Whether adults with low serum LPC concentrations are at greater risk of developing cognitive decline and AD remains a major gap in knowledge. Preventing and treating cognitive decline and the development of AD remain a major challenge. The LPC pathway is a promising area for future investigators to identify modifiable risk factors for AD.

Indexed as

Alzheimer DiseaseLysophosphatidylcholinesBrainDocosahexaenoic AcidsHumansNeuroprotectionDocosahexaenoic AcidsLysophosphatidylcholinesAlzheimer diseaseblood–brain barriercognitiondementiadocosahexaenoic acidlysophosphatidylcholinepolyunsaturated fatty acid

Identifiers

PMID32190891
PMCPMC7360459
OpenAlexW3011415530

What OpenQuestion holds

Textmetadata
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.