Evidence map›Paper›PMID 22446181›Full record

ArticleThe Journal of clinical investigation2012

Parkinson's disease: don't mess with calcium.

Mark P Mattson

Open access · bronzeAbstract readComment
In one paragraph

Article in The Journal of clinical investigation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.5field-weighted citation impact, top 12% 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

13 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Nature, Calcigender, Nurture: Sex-dependent differential CaCommunicative & integrative biology · 2019
    Review
  5. Article
  6. MPPScientific reports · 2018
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Mark P MattsonLaboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, Maryland 21224, USA. mattsonm@grc.nia.nih.gov
National Institute on Aging · US

Funding

Intramural NIH HHS
6 · The paper itself

Abstract

The hallmark of the movement disorder Parkinson's disease (PD) is progressive degeneration of dopaminergic neurons. Mitochondrial dysfunction, impaired ubiquitin-mediated proteolysis of α-synuclein, and ER stress are each implicated in the complex and poorly understood sequence of events leading to dopaminergic neuron demise. In this issue of the JCI, Selvaraj et al. report that in a mouse neurotoxin-based model of PD, reduced Ca2+ influx through transient receptor potential C1 (TRPC1) channels in the plasma membrane of dopaminergic neurons triggers a cell death-inducing ER stress response. These new findings suggest that TRPC1 channels normally function in Ca2+-mediated signaling pathways that couple adaptive/neurotrophic responses to metabolic and oxidative stress and suggest that disruption of these pathways may contribute to PD.

Indexed as

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridineAnimalsCalcium SignalingDopaminergic NeuronsEndoplasmic Reticulum StressHumansMaleParkinsonian DisordersProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesTRPC Cation ChannelsUnfolded Protein Response1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridineAkt1 protein, mousemTOR protein, mouseProto-Oncogene Proteins c-aktTOR Serine-Threonine Kinasestransient receptor potential cation channel, subfamily C, member 1TRPC Cation Channels

Identifiers

PMID22446181
PMCPMC3314478
OpenAlexW2056702299

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.