Evidence map›Paper›PMID 28273718›Full record

ReviewJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2017

Mechanisms of Parkinson's disease-related proteins in mediating secondary brain damage after cerebral ischemia.

TaeHee Kim, Raghu Vemuganti

Open access · hybridAbstract readReview
In one paragraph

Review in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
4.7field-weighted citation impact, top 5% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Review
  5. Article
  6. Reduced and Delayed Cerebrovascular Reactivity in Patients with Parkinson's Disease.Movement disorders : official journal of the Movement Disorder Society · 2023
    Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. The Potential Role of MicroRNA-124 in Cerebral Ischemia Injury.International journal of molecular sciences · 2019
    Review
  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

2 authors at 2 institutions in 1 country.

TaeHee Kim1 Department of Neurological Surgery, University of Wisconsin, Madison, WI, USA.
Raghu Vemuganti1 Department of Neurological Surgery, University of Wisconsin, Madison, WI, USA.
Neurological Surgery · USUniversity of Wisconsin–Madison · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Both Parkinson's disease (PD) and stroke are debilitating conditions that result in neuronal death and loss of neurological functions. These two conditions predominantly affect aging populations with the deterioration of the quality of life for the patients themselves and a tremendous burden to families. While the neurodegeneration and symptomology of PD develop chronically over the years, post-stroke neuronal death and dysfunction develop rapidly in days. Despite the discrepancy in the pathophysiological time frame and severity, both conditions share common molecular mechanisms that include oxidative stress, mitochondrial dysfunction, inflammation, endoplasmic reticulum stress, and activation of various cell death pathways (apoptosis/necrosis/autophagy) that synergistically modulate the neuronal death. Emerging evidence indicates that several proteins associated with early-onset familial PD play critical roles in mediating the neuronal death. Importantly, mutations in the genes encoding Parkin, PTEN-induced putative kinase 1 and DJ-1 mediate autosomal recessive forms of PD, whereas mutations in the genes encoding leucine-rich repeat kinase 2 and α-synuclein are responsible for autosomal dominant PD. This review discusses the significance of these proteins with the emphasis on the role of α-synuclein in mediating post-ischemic brain damage.

Indexed as

alpha-SynucleinApoptosisBrain IschemiaHumansLeucine-Rich Repeat Serine-Threonine Protein Kinase-2Lewy BodiesParkinson DiseaseProtein Deglycase DJ-1Protein KinasesProtein Processing, Post-TranslationalPTEN-Induced Putative KinaseUbiquitin-Protein Ligasesalpha-SynucleinLeucine-Rich Repeat Serine-Threonine Protein Kinase-2LRRK2 protein, humanPARK7 protein, humanparkin proteinProtein Deglycase DJ-1Protein KinasesPTEN-Induced Putative KinaseUbiquitin-Protein Ligasescerebral ischemianeurodegenerationneuroprotectionParkinson’s diseaseα-synuclein

Identifiers

PMID28273718
PMCPMC5444552
OpenAlexW2589589355

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.