Evidence map›Paper›PMID 30582885›Full record

ArticleBrain pathology (Zurich, Switzerland)2019

Degeneration of dopaminergic circuitry influences depressive symptoms in Lewy body disorders.

Lina Patterson, Steven P Rushton, Johannes Attems, Alan J Thomas, Christopher M Morris

Open access · hybridAbstract read
In one paragraph

Article in Brain pathology (Zurich, Switzerland), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing 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

32 citing papers in PubMed, 55 citations in OpenAlex.

  1. Review
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  14. Depression in dementia with Lewy bodies: a critical update.Journal of neural transmission (Vienna, Austria : 1996) · 2023
    Review
  15. Review
  16. Article
  17. Article
  18. The pathobiological basis of depression in Parkinson disease: challenges and outlooks.Journal of neural transmission (Vienna, Austria : 1996) · 2022
    Review
  19. Review
  20. Targeted Molecular Therapeutics for Parkinson's Disease: A Role for Antisense Oligonucleotides?Movement disorders : official journal of the Movement Disorder Society · 2022
    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 1 country.

Lina PattersonAlzheimer's Society Doctoral Training Centre, Newcastle University, Campus for Ageing and Vitality, Newcastle upon Tyne, UK.ORCID 0000-0002-9613-6601
Steven P RushtonSchool of Biology, Newcastle University, Ridley Building, Newcastle upon Tyne, UK.
Johannes AttemsAlzheimer's Society Doctoral Training Centre, Newcastle University, Campus for Ageing and Vitality, Newcastle upon Tyne, UK.
Alan J ThomasAlzheimer's Society Doctoral Training Centre, Newcastle University, Campus for Ageing and Vitality, Newcastle upon Tyne, UK.
Christopher M MorrisNIHR Biomedical Research Centre Newcastle, Biomedical Research Building, Newcastle University, Campus for Ageing and Vitality, Newcastle upon Tyne, UK.
Alzheimer's Society · GBNewcastle University · GBNIHR Newcastle Biomedical Research Centre · GB

Funding

Medical Research Council G0400074Medical Research Council G0502157Medical Research Council G0900652Medical Research Council G1100540
6 · The paper itself

Abstract

aimsDepression is commonly observed even in prodromal stages of Lewy body disorders (LBD), and is associated with cognitive impairment and a faster rate of cognitive decline. Given the role of dopamine in the development of movement disorders, but also in motivation and reward, we investigated neurodegenerative pathology in dopaminergic circuitry in Parkinson's disease (PD), PD with dementia (PDD) and dementia with Lewy bodies (DLB) patients in relation to depressive symptoms.

methodsα-synuclein, hyperphosphorylated tau and amyloid-beta pathology was assessed in 17 DLB, 14 PDD and 8 PD cases within striatal and midbrain subregions, with neuronal cell density assessed in substantia nigra and ventral tegmental area. Additionally, we used a structural equation modeling (SEM) approach to investigate the extent to which brain connectivity might influence the deposition of pathological proteins within dopaminergic pathways.

resultsA significantly higher α-synuclein burden was observed in the substantia nigra (P = 0.006), ventral tegmental area (P = 0.011) and nucleus accumbens (P = 0.031) in LBD patients with depression. Significant negative correlations were observed between cell density in substantia nigra with Lewy body (LB) Braak stage (P = 0.013), whereas cell density in ventral tegmental area showed negative correlations with LB Braak stage (P = 0.026) and neurofibrillary tangle Braak stage (P = 0.007).

conclusionsDopaminergic α-synuclein pathology appears to drive depression. Selective targeting of dopaminergic pathways may therefore provide symptomatic relief for depressive symptoms in LBD patients.

Indexed as

Agedalpha-SynucleinAmyloid beta-PeptidesBrainDementiaDepressionDopaminergic NeuronsFemaleHumansInclusion BodiesLewy BodiesLewy Body DiseaseMaleNeurofibrillary TanglesNeuronsParkinson Diseasealpha-SynucleinAmyloid beta-Peptidestau Proteinsdementia with Lewy bodiesdepressiondopaminergic pathwaysα-synuclein

Identifiers

PMID30582885
PMCPMC6767514
OpenAlexW2906213111

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Registered trials

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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.