Evidence map›Paper›PMID 36322206›Full record

ReviewJournal of neural transmission (Vienna, Austria : 1996)2022

The pathobiological basis of depression in Parkinson disease: challenges and outlooks.

Kurt A Jellinger

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of neural transmission (Vienna, Austria : 1996), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
5.6field-weighted citation impact, top 3% 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, 51 citations in OpenAlex.

  1. Trial
  2. Psilocybin therapy for mood dysfunction in Parkinson's disease: an open-label pilot trial.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025
    Trial
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Cognitive impairment in Parkinson's disease and other parkinsonian syndromes.Journal of neural transmission (Vienna, Austria : 1996) · 2025
    Review
  15. Behavioral disorders in Parkinson disease: current view.Journal of neural transmission (Vienna, Austria : 1996) · 2025
    Review
  16. Review
  17. Article
  18. The pathobiology of depression in Huntington's disease: an unresolved puzzle.Journal of neural transmission (Vienna, Austria : 1996) · 2024
    Review
  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

1 author at 1 institution in 1 country.

Kurt A JellingerInstitute of Clinical Neurobiology, Alberichgasse 5/13, 1150, Vienna, Austria. kurt.jellinger@univie.ac.at.ORCID 0000-0002-9641-7649
University of Vienna · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Depression, with an estimated prevalence of about 40% is a most common neuropsychiatric disorder in Parkinson disease (PD), with a negative impact on quality of life, cognitive impairment and functional disability, yet the underlying neurobiology is poorly understood. Depression in PD (DPD), one of its most common non-motor symptoms, can precede the onset of motor symptoms but can occur at any stage of the disease. Although its diagnosis is based on standard criteria, due to overlap with other symptoms related to PD or to side effects of treatment, depression is frequently underdiagnosed and undertreated. DPD has been related to a variety of pathogenic mechanisms associated with the underlying neurodegenerative process, in particular dysfunction of neurotransmitter systems (dopaminergic, serotonergic and noradrenergic), as well as to disturbances of cortico-limbic, striato-thalamic-prefrontal, mediotemporal-limbic networks, with disruption in the topological organization of functional mood-related, motor and other essential brain network connections due to alterations in the blood-oxygen-level-dependent (BOLD) fluctuations in multiple brain areas. Other hypothetic mechanisms involve neuroinflammation, neuroimmune dysregulation, stress hormones, neurotrophic, toxic or metabolic factors. The pathophysiology and pathogenesis of DPD are multifactorial and complex, and its interactions with genetic factors, age-related changes, cognitive disposition and other co-morbidities awaits further elucidation.

Indexed as

Cognitive DysfunctionParkinson DiseaseBrainDepressionHumansQuality of LifeBrain network disconnectionsDepressionNeuroimagingNeuropathologyNeurotransmitter dysfunctionsParkinson disease

Identifiers

PMID36322206
PMCPMC9628588
OpenAlexW4308113930

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.