Evidence map›Paper›PMID 15717003›Full record

ReviewNeuroRx : the journal of the American Society for Experimental NeuroTherapeutics2004

Mechanisms of neural cell death: implications for development of neuroprotective treatment strategies.

Alexander G Yakovlev, Alan I Faden

Registry-linked trialAbstract readReview
In one paragraph

Review in NeuroRx : the journal of the American Society for Experimental NeuroTherapeutics, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06537713 (Diagnostic Role of Serum Testican and Ubiquitin Levels in Patients With Head Trauma), which is not on this map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
–field-weighted citation impact
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.

NCT06537713 completednot on this mapstarted 2020, after this paper: background citation

Diagnostic Role of Serum Testican and Ubiquitin Levels in Patients With Head Trauma

TypeobservationalSponsorKanuni Sultan Suleyman Training and Research HospitalRan2020 to 2021Enrolled89ConditionsModerate Traumatic Brain Injury, Testican-1, UbiquitinArmsTestican-1
3 · Its place in the literature

Who cites it

46 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
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  8. Review
  9. Article
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  12. Article
  13. International journal of molecular sciences · 2020
    Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  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

2 authors.

Alexander G YakovlevDepartment of Neuroscience, Georgetown University Medical Center, Washington, DC 20057, USA.
Alan I Faden

Funding

NEUROIMAGING COREP30HD040677 · NICHD · CHILDREN'S RESEARCH INSTITUTE · PI VITTORIO GALLO, VITTORIO GALLO VITTORIO GALLO · 2001 to 2015
$15.9M
APOPTOSIS INDUCED BY TRAUMATIC BRAIN INJURYR01NS036537 · NINDS · GEORGETOWN UNIVERSITY · PI FADEN, ALAN IRA · 1998 to 2005
$1.6M
MULTIPONTENTIAL DRUG TREATMENT STRATEGIES IN NEUROTRAMAR01NS041119 · NINDS · GEORGETOWN UNIVERSITY · PI FADEN, ALAN IRA · 2000 to 2002
$973k
REGULATION OF CASPASE 3 GENE EXPRESSION IN NEURONAL CELLR01NS038941 · NINDS · GEORGETOWN UNIVERSITY · PI YAKOVLEV, ALEXANDER G · 1999 to 2001
$257k
NICHD NIH HHS P30 HD040677NICHD NIH HHS P30 HD40677NINDS NIH HHS R01 NS036537NINDS NIH HHS R01 NS041119NINDS NIH HHS R01 NS36537NINDS NIH HHS R01 NS38941NINDS NIH HHS R01 NS41119
6 · The paper itself

Abstract

It has been increasingly recognized that cell death phenotypes and their molecular mechanisms are highly diverse. Necrosis is no longer considered a single entity, passively mediated by energy failure. Moreover, caspase-dependent apoptosis is not the only pathway involved in programmed cell death or even the only apoptotic mechanism. Recent experimental work emphasizes the diverse and interrelated nature of cell death mechanisms. Thus, there are both caspase-dependent and caspase-independent forms of apoptosis, which may differ morphologically as well as mechanistically. There are also necrotic-like phenotypes that require de novo protein synthesis and are, therefore, forms of programmed cell death. In addition, forms of cell death showing certain morphological features of both necrosis and apoptosis have been identified, leading to the term aponecrosis. Considerable experimental evidence also shows that modulation of one form of cell death may lead to another. Together, these observations underscore the need to substantially revise our conceptions about neuroprotection strategies. Use of multiple treatments that target different cell death cascades, or single agents that moderate multiple cell death pathways, is likely to lead to more effective neuroprotection for clinical disorders.

Indexed as

Neuroprotective AgentsAnimalsBrainCell DeathHumansNeuronsNeuroprotective Agents

Identifiers

PMID15717003
PMCPMC534908

What OpenQuestion holds

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Read underepoch 390

Registered trials

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.