Evidence map›Paper›PMID 26954980›Full record

ReviewTranslational psychiatry2016

What can rodent models tell us about apathy and associated neuropsychiatric symptoms in Parkinson's disease?

R Magnard, Y Vachez, C Carcenac, P Krack, O David, M Savasta, S Boulet, S Carnicella

Open access · goldAbstract readReview
In one paragraph

Review in Translational psychiatry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 2 pooled it
4.0field-weighted citation impact, top 6% 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

35 citing papers in PubMed, 2 syntheses or guidelines pooled it, 72 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Article
  6. Article
  7. Behavioral disorders in Parkinson disease: current view.Journal of neural transmission (Vienna, Austria : 1996) · 2025
    Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Architecture of the subthalamic nucleus.Communications biology · 2024
    Review
  13. Review
  14. Article
  15. The pathobiological basis of depression in Parkinson disease: challenges and outlooks.Journal of neural transmission (Vienna, Austria : 1996) · 2022
    Review
  16. Article
  17. Review
  18. Article
  19. Review
  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

8 authors at 3 institutions in 1 country.

R MagnardInserm U1216, Grenoble, France.
Y VachezInserm U1216, Grenoble, France.
C CarcenacInserm U1216, Grenoble, France.
P KrackInserm U1216, Grenoble, France.
O DavidInserm U1216, Grenoble, France.
M SavastaInserm U1216, Grenoble, France.
S BouletInserm U1216, Grenoble, France.
S CarnicellaInserm U1216, Grenoble, France.
Grenoble Institute of Neurosciences · FRInserm · FRUniversité Grenoble Alpes · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In addition to classical motor symptoms, Parkinson's disease (PD) patients display incapacitating neuropsychiatric manifestations, such as apathy, anhedonia, depression and anxiety. These hitherto generally neglected non-motor symptoms, have gained increasing interest in medical and scientific communities over the last decade because of the extent of their negative impact on PD patients' quality of life. Although recent clinical and functional imaging studies have provided useful information, the pathophysiology of apathy and associated affective impairments remains elusive. Our aim in this review is to summarize and discuss recent advances in the development of rodent models of PD-related neuropsychiatric symptoms using neurotoxin lesion-based approaches. The data collected suggest that bilateral and partial lesions of the nigrostriatal system aimed at inducing reliable neuropsychiatric-like deficits while avoiding severe motor impairments that may interfere with behavioral evaluation, is a more selective and efficient strategy than medial forebrain bundle lesions. Moreover, of all the different classes of pharmacological agents, D2/D3 receptor agonists such as pramipexole appear to be the most efficient treatment for the wide range of behavioral deficits induced by dopaminergic lesions. Lesion-based rodent models, therefore, appear to be relevant tools for studying the pathophysiology of the non-motor symptoms of PD. Data accumulated so far confirm the causative role of dopaminergic depletion, especially in the nigrostriatal system, in the development of behavioral impairments related to apathy, depression and anxiety. They also put forward D2/D3 receptors as potential targets for the treatment of such neuropsychiatric symptoms in PD.

Indexed as

AnhedoniaApathyAnimalsAnxietyBehavior, AnimalBenzothiazolesDepressionDisease Models, AnimalDopamine AgonistsMiceNeostriatumParkinson DiseasePramipexoleRatsReceptors, Dopamine D2Receptors, Dopamine D3BenzothiazolesDopamine AgonistsPramipexoleReceptors, Dopamine D2Receptors, Dopamine D3

Identifiers

PMID26954980
PMCPMC4872443
OpenAlexW2296450808

What OpenQuestion holds

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LicenceCC BY
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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.