Evidence map›Paper›PMID 40024917›Full record

ArticleActa neuropathologica2025

Evidence of COMT dysfunction in the olfactory bulb in Parkinson's disease.

Leah C Beauchamp, Laura J Ellett, Sydney M A Juan, Xiang M Liu, Cameron P J Hunt, Clare L Parish, Laura H Jacobson, Claire E Shepherd, Glenda M Halliday, Ashley I Bush and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Acta neuropathologica, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Olfaction function improves in a specialised unit for Parkinson's disease.Journal of neural transmission (Vienna, Austria : 1996) · 2026
    Observational
  2. 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

13 authors.

Leah C BeauchampAnn Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, 02115, USA.
Laura J EllettThe Florey Institute of Neuroscience and Mental Health, and The University of Melbourne, Parkville, VIC, 3052, Australia.
Sydney M A JuanThe Florey Institute of Neuroscience and Mental Health, and The University of Melbourne, Parkville, VIC, 3052, Australia.
Xiang M LiuThe Florey Institute of Neuroscience and Mental Health, and The University of Melbourne, Parkville, VIC, 3052, Australia.
Cameron P J HuntThe Florey Institute of Neuroscience and Mental Health, and The University of Melbourne, Parkville, VIC, 3052, Australia.
Clare L ParishThe Florey Institute of Neuroscience and Mental Health, and The University of Melbourne, Parkville, VIC, 3052, Australia.
Laura H JacobsonThe Florey Institute of Neuroscience and Mental Health, and The University of Melbourne, Parkville, VIC, 3052, Australia.
Claire E ShepherdNeuroscience Research Australia, Sydney, NSW, 2031, Australia.
Glenda M HallidayFaculty of Medicine and Health, School of Medical Sciences, University of Sydney Brain and Mind Centre, Camperdown, NSW, Australia.
Ashley I BushThe Florey Institute of Neuroscience and Mental Health, and The University of Melbourne, Parkville, VIC, 3052, Australia.
Laura J VellaThe Florey Institute of Neuroscience and Mental Health, and The University of Melbourne, Parkville, VIC, 3052, Australia.
David I FinkelsteinThe Florey Institute of Neuroscience and Mental Health, and The University of Melbourne, Parkville, VIC, 3052, Australia.
Kevin J BarnhamThe Florey Institute of Neuroscience and Mental Health, and The University of Melbourne, Parkville, VIC, 3052, Australia. kbarnham@unimelb.edu.au.

Funding

National Health and Medical Research Council GNT1194028
6 · The paper itself

Abstract

Hyposmia is one of the most prevalent non-motor symptoms of Parkinson's disease and antecedes motor dysfunction by up to a decade. However, the underlying pathophysiology remains poorly understood. In this study, we investigated the mechanisms of dopamine metabolism in post-mortem olfactory bulbs from ten Parkinson's disease and ten neurologic control subjects. In contrast to the loss of dopaminergic neurons in the midbrain, we observed an increase in tyrosine hydroxylase-positive neurons in the Parkinson's disease olfactory bulb, suggesting a potential role for dopamine in the hyposmia associated with the condition. Using immunohistochemistry, high-performance liquid chromatography, western blot, and enzyme-linked immunosorbent assays, we demonstrate a reduction in catechol-O-methyltransferase catabolism of dopamine to homovanillic acid, potentially due to a depletion of the methyl donor substrate S-adenosyl methionine. We hypothesized that reduction in catechol-O-methyltransferase activity would result in increased dopamine occupation of the D

Indexed as

AnosmiaCatechol O-MethyltransferaseOlfactory BulbParkinson DiseaseAgedAged, 80 and overAnimalsDisease Models, AnimalDopamineDopamine D2 Receptor AntagonistsDopaminergic NeuronsFemaleHaloperidolHomovanillic AcidHumansMaleCatechol O-MethyltransferaseCOMT protein, humanCOMT protein, mouseDopamineDopamine D2 Receptor AntagonistsHaloperidolHomovanillic AcidReceptors, Dopamine D2tau ProteinsCatechol-O-methyltransferaseDopamineHyposmiaOlfactionParkinson’s disease

Identifiers

PMID40024917
PMCPMC11872990

What OpenQuestion holds

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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.