Evidence map›Paper›PMID 16077186›Full record

ReviewMolecular neurobiology2005

Lipid signaling in neural plasticity, brain repair, and neuroprotection.

Nicolas G Bazan

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular neurobiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed, 1 pooled it
13.4field-weighted citation impact, top 1% 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

78 citing papers in PubMed, 1 synthesis or guideline pooled it, 238 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. White matter lipidome alterations in the schizophrenia brain.Schizophrenia (Heidelberg, Germany) · 2024
    Article
  10. Article
  11. Article
  12. Lipidome atlas of the adult human brain.Nature communications · 2024
    Article
  13. Article
  14. Article
  15. Article
  16. Lipid Profiling in Alzheimer's Disease.Advances in experimental medicine and biology · 2023
    Article
  17. Review
  18. Synergistic Neuroprotection by a PAF Antagonist Plus a Docosanoid in Experimental Ischemic Stroke: Dose-Response and Therapeutic Window.Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association · 2022
    Article
  19. Article
  20. Article

18 more citing papers are in PubMed but not listed here.

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.

Nicolas G BazanLSU Neuroscience Center of Excellence and Department of Ophthalmology, Louisiana State University Health Sciences Center, New Orleans, LA, USA. nbazan@lsuhsc.edu
Louisiana State University Health Sciences Center New Orleans · US

Funding

NCRR NIH HHS P20RR16816NEI NIH HHS EY05121NINDS NIH HHS NS23002NINDS NIH HHS NS46741
6 · The paper itself

Abstract

The extensive networking of the cells of the nervous system results in large cell membrane surface areas. We now know that neuronal membranes contain phospholipid pools that are the reservoirs for the synthesis of specific lipid messengers on neuronal stimulation or injury. These messengers in turn participate in signaling cascades that can either promote neuronal injury or neuroprotection. Prostaglandins are synthesized as a result of cyclooxygenase activity. In the first step of the arachidonic acid cascade, the short-lived precursor, prostaglandin H2, is synthesized. Additional steps in the cascade result in the synthesis of an array of prostaglandins, which participate in numerous physiological and neurological processes. Our laboratory recently reported that the membrane polyunsaturated fatty acid, docosahexaenoic acid, is the precursor of oxygenation products now known as the docosanoids, some of which are powerful counter-proinflammatory mediators. The mediator 10,17S-docosatriene (neuroprotectin D1, NPD1) counteracts leukocyte infiltration, NF-kappa activation, and proinflammatory gene expression in brain ischemia-reperfusion and is an apoptostatic mediator, potently counteracting oxidative stress-triggered apoptotic DNA damage in retinal pigment epithelial cells. NPD1 also upregulates the anti-apoptotic proteins Bcl-2 and Bcl-xL and decreases pro-apoptotic Bax and Bad expression. Another biologically active messenger derived from membrane phospholipids in response to synaptic activity is platelet-activating factor (PAF). The tight regulation of the balance between synthesis (via phospholipases) and degradation (via acetylhydrolases) of PAF modulates the functions of this lipid messenger. Under pathological conditions, this balance is tipped, and PAF becomes a proinflammatory mediator and neurotoxic agent. The newly discovered docosahexaenoic acid signaling pathways, as well as other lipid messengers related to synaptic activation, may lead to the clarification of clinical issues relevant to stroke, age-related macular degeneration, spinal cord injury, Alzheimer's disease, and other diseases that include neuroinflammatory components.

Indexed as

Nervous System Physiological PhenomenaAnimalsCell SurvivalHumansLipidsNeuronal PlasticityNeuronsNeuroprotective AgentsProstaglandinsSignal TransductionLipidsNeuroprotective AgentsProstaglandins

Identifiers

PMID16077186
OpenAlexW2046734045

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.