Evidence map›Paper›PMID 21615738›Full record

ReviewJournal of neurochemistry2011

Tracking extranigral degeneration in animal models of Parkinson's disease: quest for effective therapeutic strategies.

Varduhi H Knaryan, Supriti Samantaray, Charlene Le Gal, Swapan K Ray, Naren L Banik

Abstract readReview
In one paragraph

Review in Journal of neurochemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

11 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Aging, circadian rhythms and depressive disorders: a review.American journal of neurodegenerative disease · 2013
    Review
  10. Regional, kinetic [(18)F]FDG PET imaging of a unilateral Parkinsonian animal model.American journal of nuclear medicine and molecular imaging · 2013
    Article
  11. 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

5 authors at 3 institutions in 2 countries.

Varduhi H KnaryanDepartment of Neurosciences, Medical University of South Carolina, Charleston, South Carolina, USA.
Supriti Samantaray
Charlene Le Gal
Swapan K Ray
Naren L Banik
Medical University of South Carolina · USUniversité de Poitiers · FRUniversity of South Carolina · US

Funding

Extra-nigral Neurodegeneration in Experimental Parkinson's DiseaseR01NS062327 · NINDS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI BANIK, NAREN L · 2009 to 2013
$1.6M
NINDS NIH HHS R01 NS062327NINDS NIH HHS R01 NS62327
6 · The paper itself

Abstract

Sporadic Parkinson's disease (PD) is now interpreted as a complex nervous system disorder in which the projection neurons are predominantly damaged. Such an interpretation is based on mapping of Lewy body and Lewy neurite pathology. Symptoms of the human disease are much widespread, which span from pre-clinical non-motor symptoms and clinical motor symptoms to cognitive discrepancies often seen in advanced stages. Existing symptomatic treatments further complicate with overt drug-irresponsive symptoms. PD is better understood by assimilation of extranigral degenerative pathways with nigrostriatal degenerative mechanisms. The term 'extranigral' appeared first in the 1990s to more rigorously define the nigral pathology by process of elimination. However, as clinicians progressively identified PD symptoms unresponsive to the gold standard drug l-DOPA, definitions of PD symptoms were redefined. Non-motor symptoms prodromal to motor symptoms just as pre-clinical to clinical, and conjointly emerged the concept of nigral versus extranigral degeneration in PD. While nigrostriatal degeneration is responsible for the neurobiological substrates of extrapyramydal motor features, extranigral degeneration corroborates a vast majority of other changes in discrete central, peripheral, and enteric nervous system nuclei, which together account for global symptoms of the human disease. As an extranigral site, spinal cord degeneration has also been implicated in PD progression. Interconnected to the upper CNS structures with descending and ascending pathways, spinal neurons participate in movement and sensory circuits, controlling movement and reflexes. Several clinical and in vivo studies have demonstrated signs of parkinsonism-related degenerative processes in spinal cord, which led to recent consideration of spinal cord as an area of potential therapeutic target. In a nutshell, this review explores how the existing animal models can actually reflect the human disease in order to facilitate PD research. Evolution of extranigral degeneration studies has been succinctly revisited, followed by a survey on animal models in light of recent findings in clinical PD. Together, it may help to develop effective therapeutic strategies for PD.

Indexed as

AnimalsAntiparkinson AgentsCentral Nervous SystemDisease Models, AnimalDogsHumansMiceNerve DegenerationParkinson DiseasePrimatesRatsSpinal CordSubstantia NigraAntiparkinson Agents

Identifiers

PMID21615738
PMCPMC3135734
OpenAlexW1514033836

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.