Evidence map›Paper›PMID 25697885›Full record

ArticleNeuromolecular medicine2015

Unfolding the promise of translational targeting in neurodegenerative disease.

Thomas M Drake

Abstract read
PubMed Publisher
In one paragraph

Article in Neuromolecular medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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.

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

3 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
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.

Thomas M DrakeAcademic Unit of Surgical Oncology, The Medical School, University of Sheffield, Sheffield, S10 2RX, UK, tmdrake1@sheffield.ac.uk.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

With the rise of aging populations, new challenges for health care systems are emerging. Degenerative conditions of the central nervous system share a strikingly great deal of similarities, particularly the production and buildup of malfolded proteins. As a result, stress pathways within the endoplasmic reticulum become activated, triggering widespread neuronal apoptosis. New pharmacological compounds targeting this response are emerging as promising treatment strategies. This review examines the current evidence for protein aggregation in neurodegenerative disease states and discusses future mechanisms of therapeutically targeting the endoplasmic reticulum.

Indexed as

Molecular Targeted TherapyActivating Transcription Factor 6AgingAnimalsApoptosisCellular MicroenvironmentDantroleneDisease ProgressioneIF-2 KinaseEndoplasmic ReticulumEndoplasmic Reticulum Chaperone BiPEndoplasmic Reticulum StressEndoribonucleasesHeat-Shock ProteinsHSP90 Heat-Shock ProteinsHumansActivating Transcription Factor 6DantroleneeIF-2 KinaseEndoplasmic Reticulum Chaperone BiPEndoribonucleasesERN1 protein, humanHeat-Shock ProteinsHSP90 Heat-Shock ProteinsLipoxygenase InhibitorsMinocyclineMolecular ChaperonesNerve Tissue ProteinsNeuroprotective AgentsProtein Kinase InhibitorsProtein Serine-Threonine Kinases

Identifiers

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.