Evidence map›Paper›PMID 21196395›Full record

ReviewFrontiers in bioscience (Scholar edition)2011

Protective mechanisms by cystatin C in neurodegenerative diseases.

Sebastien Gauthier, Gurjinder Kaur, Weiqian Mi, Belen Tizon, Efrat Levy

Open access · bronzeAbstract readReview
In one paragraph

Review in Frontiers in bioscience (Scholar edition), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 11% 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

73 citing papers in PubMed, 1 synthesis or guideline pooled it, 123 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Serum Cystatin C is a potential biomarker for predicting amyotrophic lateral sclerosis survival.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2024
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Effect of Ovocystatin on Amyloid β 1-42 Aggregation-In Vitro Studies.International journal of molecular sciences · 2023
    Article
  17. Review
  18. Article
  19. Article
  20. Article

13 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

5 authors at 1 institution in 1 country.

Sebastien GauthierNathan S. Kline Institute, Orangeburg, NY 10962, USA.
Gurjinder Kaur
Weiqian Mi
Belen Tizon
Efrat Levy
Nathan Kline Institute for Psychiatric Research · US

Funding

Uncovering Alzheimer's disease risk mechanisms through neuron-specific analysis of autophagy and endosomal-lysosomal functionP01AG017617 · NIA · NATHAN S. KLINE INSTITUTE FOR PSYCH RES · PI NIXON, RALPH A. · 2000 to 2021
$40.0M
Animal models for cerebral amyloid angiopathyR01NS042029 · NINDS · NATHAN S. KLINE INSTITUTE FOR PSYCH RES · PI LEVY, EFRAT · 2002 to 2006
$1.5M
NIA NIH HHS AG017617NIA NIH HHS P01 AG017617NINDS NIH HHS NS42029NINDS NIH HHS R01 NS042029
6 · The paper itself

Abstract

Neurodegeneration occurs in acute pathological conditions such as stroke, ischemia, and head trauma and in chronic disorders such as Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis. While the cause of neuronal death is different and not always known in these varied conditions, hindrance of cell death would be beneficial in the prevention of, slowing of, or halting disease progression. Enhanced cystatin C (CysC) expression in these conditions caused a debate as to whether CysC up-regulation facilitates neurodegeneration or it is an endogenous neuroprotective attempt to prevent the progression of the pathology. However, recent in vitro and in vivo data have demonstrated that CysC plays protective roles via pathways that are dependent on inhibition of cysteine proteases, such as cathepsin B, or by induction of autophagy, induction of proliferation, and inhibition of amyloid-beta aggregation. Here we review the data demonstrating the protective roles of CysC under conditions of neuronal challenge and the protective pathways induced under various conditions. These data suggest that CysC is a therapeutic candidate that can potentially prevent brain damage and neurodegeneration.

Indexed as

CytoprotectionAmyloidAnimalsAutophagyBrainCystatin CCysteine Proteinase InhibitorsGene Expression RegulationHumansMiceNeurodegenerative DiseasesNeurogenesisNeuroprotective AgentsAmyloidCystatin CCysteine Proteinase InhibitorsNeuroprotective Agents

Identifiers

PMID21196395
PMCPMC3038625
OpenAlexW1974739417

What OpenQuestion holds

Textmetadata
LicenceTDM
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.