Evidence map›Paper›PMID 29254095›Full record

ReviewJournal of Alzheimer's disease : JAD2018

Dissecting the Role of 5-Lipoxygenase in the Homocysteine-Induced Alzheimer's Disease Pathology.

Antonio Di Meco, Jian-Guo Li, Domenico Praticò

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of Alzheimer's disease : JAD, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.9field-weighted citation impact, top 24% 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

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Controlling the Impact ofMedicina (Kaunas, Lithuania) · 2023
    Article
  6. Article
  7. Article
  8. Review
  9. Review
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  11. 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

3 authors at 1 institution in 1 country.

Antonio Di MecoAlzheimer's Center at Temple, Lewis Katz School of Medicine Temple University, Philadelphia, PA, USA.
Jian-Guo LiAlzheimer's Center at Temple, Lewis Katz School of Medicine Temple University, Philadelphia, PA, USA.
Domenico PraticòAlzheimer's Center at Temple, Lewis Katz School of Medicine Temple University, Philadelphia, PA, USA.
Temple University · US

Funding

Dissecting the role of 5LO in neurodegeneration associated with homocysteineRF1AG051684 · NIA · TEMPLE UNIV OF THE COMMONWEALTH · PI PRATICO, DOMENICO · 2016 to 2016
$1.9M
5Lipoxygenase-mediated vasculopathy in HHcyR01HL112966 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI PRATICO, DOMENICO · 2013 to 2016
$1.5M
NHLBI NIH HHS R01 HL112966NIA NIH HHS RF1 AG051684
6 · The paper itself

Abstract

Alzheimer's disease (AD) affects over 40 million patients around the world and poses a huge economic burden on society since no effective therapy is available yet. While the cause(s) for the most common sporadic form of the disease are still obscure, lifestyle and different environmental factors have emerged as modulators of AD susceptibility. Hyperhomocysteinemia (HHCY), a condition of high circulating levels of homocysteine, is an independent but modifiable risk factor for AD. Studies in AD mouse models have linked HHCY with memory impairment, amyloidosis, tau pathology, synaptic dysfunction, and neuroinflammation. However, the exact mechanism by which HHCY affects AD pathogenesis is unclear. The 5-lipoxygenase (5LO) is a protein upregulated in postmortem AD brains and plays a functional role in AD pathogenesis. Recently, in vitro and in vivo studies showed that HHCY effects on amyloid-β and tau pathology, synapse and memory impairments are dependent on the activation of the 5LO enzymatic pathway, since its genetic absence or pharmacological inhibition prevents them. HHCY induces 5LO gene upregulation by lowering the methylation of its promoter, which results in increased translation and transcription of its mRNA. Based on these findings, we propose that epigenetic modification of 5LO represents the missing biological link between HHCY and AD pathogenesis, and for this reason it represents a viable therapeutic target to prevent AD development in individuals bearing this risk factor.

Indexed as

Alzheimer DiseaseAnimalsArachidonate 5-LipoxygenaseBrainEpigenesis, GeneticHomocysteineHumansHyperhomocysteinemiaArachidonate 5-LipoxygenaseHomocysteineAlzheimer’s diseaseamyloid-βfive-lipoxygenasehomocysteinesynapsetau protein

Identifiers

PMID29254095
PMCPMC5869997
OpenAlexW2773940808

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.