Evidence map›Paper›PMID 22476944›Full record

ReviewMolecular neurobiology2012

Integrating cytosolic phospholipase A₂ with oxidative/nitrosative signaling pathways in neurons: a novel therapeutic strategy for AD.

Grace Y Sun, Yan He, Dennis Y Chuang, James C Lee, Zezong Gu, Agnes Simonyi, Albert Y Sun

Open access · greenAbstract readReview
In one paragraph

Review in Molecular neurobiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

28 citing papers in PubMed, 43 citations in OpenAlex.

  1. A perspective: PLA2G4A as drug target for vascular inflammation in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Review
  2. Development of potent, selective cPLAnpj drug discovery · 2026
    Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Calcium-dependent cytosolic phospholipase AMolecular neurodegeneration · 2022
    Article
  11. Review
  12. Article
  13. Review
  14. Cytosolic Phospholipase AMolecular neurobiology · 2019
    Article
  15. Edema Induced by aInternational journal of molecular sciences · 2018
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

7 authors at 1 institution in 1 country.

Grace Y SunDepartment of Biochemistry, University of Missouri, 117 Schweitzer Hall, Columbia, MO 65211, USA. sung@missouri.edu
Yan He
Dennis Y Chuang
James C Lee
Zezong Gu
Agnes Simonyi
Albert Y Sun
University of Missouri · US

Funding

PATHOGENESIS OF PHOSPHOLIPASES A2 IN ADP01AG018357 · NIA · UNIVERSITY OF MISSOURI-COLUMBIA · PI SUN, GRACE Y · 2001 to 2012
$10.4M
The Interactions Core/Mark McintoshP50AT006273 · NCCIH · UNIVERSITY OF MISSOURI-COLUMBIA · PI LUBAHN, DENNIS B · 2010 to 2014
$7.4M
NCCIH NIH HHS 1P50 AT006273NCCIH NIH HHS P50 AT006273NIA NIH HHS P01 AG018357NIA NIH HHS P02 AG018357
6 · The paper itself

Abstract

The pathophysiology of Alzheimer's disease (AD) is comprised of complex metabolic abnormalities in different cell types in the brain. To date, there are not yet effective drugs that can completely inhibit the pathophysiological event, and efforts have been devoted to prevent or minimize the progression of this disease. Much attention has focused on studies to understand aberrant functions of the ionotropic glutamate receptors, perturbation of calcium homeostasis, and toxic effects of oligomeric amyloid beta peptides (Aβ) which results in production of reactive oxygen and nitrogen species and signaling pathways, leading to mitochondrial dysfunction and synaptic impairments. Aberrant phospholipase A(2) (PLA(2)) activity has been implicated to play a role in the pathogenesis of many neurodegenerative diseases, including AD. However, mechanisms for their modes of action and their roles in the oxidative and nitrosative signaling pathways have not been firmly established. In this article, we review recent studies providing a metabolic link between cytosolic PLA(2) (cPLA(2)) and neuronal excitation due to stimulation of ionotropic glutamate receptors and toxic Aβ peptides. The requirements for Ca(2+) binding together with its posttranslational modifications by protein kinases and possible by the redox-based S-nitrosylation, provide strong support for a dynamic role of cPLA(2) in serving multiple functions to neurons and glial cells under abnormal physiological and pathological conditions. Therefore, understanding mechanisms for cPLA(2) in the oxidative and nitrosative pathways in neurons will allow the development of novel therapeutic targets to mitigate the detrimental effects of AD.

Indexed as

Signal TransductionAlzheimer DiseaseAnimalsHumansNeuronsPhospholipases A2, CytosolicReactive Nitrogen SpeciesReactive Oxygen SpeciesPhospholipases A2, CytosolicReactive Nitrogen SpeciesReactive Oxygen Species

Identifiers

PMID22476944
PMCPMC3427407
OpenAlexW2164390570

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.