Evidence map›Paper›PMID 39957584›Full record

ArticleAnnals of clinical and translational neurology2025

Amygdala Neurodegeneration: A Key Driver of Visual Dysfunction in Parkinson's Disease.

Asier Erramuzpe, Ane Murueta-Goyena, Antonio Jimenez-Marin, Marian Acera, Sara Teijeira-Portas, Rocío Del Pino, Tamara Fernández-Valle, Ibai Diez, Unai Sainz-Lugarezaresti, Naroa Ibarretxe-Bilbao and 6 more

Abstract read
In one paragraph

Article in Annals of clinical and translational neurology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Combined Dysfunction of the Amygdala and Nucleus Basalis Underlies Visual Hallucinations in Parkinson's Disease.Movement disorders : official journal of the Movement Disorder Society · 2025
    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

16 authors.

Asier ErramuzpeComputational Neuroimaging Group, Biobizkaia Health Research Institute, Barakaldo, Spain.ORCID 0000-0002-9402-2184
Ane Murueta-GoyenaNeurodegenerative Diseases Group, Biobizkaia Health Research Institute, Barakaldo, Bizkaia, Spain.ORCID 0000-0002-9808-6943
Antonio Jimenez-MarinComputational Neuroimaging Group, Biobizkaia Health Research Institute, Barakaldo, Spain.ORCID 0000-0002-6053-6101
Marian AceraNeurodegenerative Diseases Group, Biobizkaia Health Research Institute, Barakaldo, Bizkaia, Spain.ORCID 0000-0002-8333-0659
Sara Teijeira-PortasNeurodegenerative Diseases Group, Biobizkaia Health Research Institute, Barakaldo, Bizkaia, Spain.ORCID 0000-0002-2208-5864
Rocío Del PinoNeurodegenerative Diseases Group, Biobizkaia Health Research Institute, Barakaldo, Bizkaia, Spain.ORCID 0000-0002-6612-4757
Tamara Fernández-ValleNeurodegenerative Diseases Group, Biobizkaia Health Research Institute, Barakaldo, Bizkaia, Spain.ORCID 0000-0001-5666-0022
Ibai DiezComputational Neuroimaging Group, Biobizkaia Health Research Institute, Barakaldo, Spain.ORCID 0000-0001-5769-0178
Unai Sainz-LugarezarestiComputational Neuroimaging Group, Biobizkaia Health Research Institute, Barakaldo, Spain.ORCID 0009-0008-0470-5960
Naroa Ibarretxe-BilbaoDepartment of Psychology, Faculty of Health Sciences, University of Deusto, Bilbao, Spain.ORCID 0000-0002-2434-5252
Unai AyalaBiomedical Engineering Department, Faculty of Engineering, Mondragon University, Mondragon, Spain.ORCID 0000-0003-1079-752X
Maitane BarrenecheaBiomedical Engineering Department, Faculty of Engineering, Mondragon University, Mondragon, Spain.ORCID 0000-0003-0149-6944
Alberto Cabrera-ZubizarretaOSATEK Magnetic Resonance Imaging Unit, Galdakao Hospital, Galdakao, Spain.ORCID 0000-0002-1028-3521
Jesús CortésComputational Neuroimaging Group, Biobizkaia Health Research Institute, Barakaldo, Spain.ORCID 0000-0002-9059-8194
Juan Carlos Gómez-EstebanNeurodegenerative Diseases Group, Biobizkaia Health Research Institute, Barakaldo, Bizkaia, Spain.ORCID 0000-0002-4697-3890
Iñigo GabilondoBilbao, Spain.ORCID 0000-0001-6045-2840

Funding

Berrikuntza + Ikerketa + Osasuna Eusko Fundazioa 2016111009Berrikuntza + Ikerketa + Osasuna Eusko Fundazioa 2020333033Eusko Jaurlaritza PRE_2019_1_0070Ikerbasque, Basque Foundation for ScienceInstituto de Salud Carlos III JR15/00008Instituto de Salud Carlos III PI14/00679Instituto de Salud Carlos III PI16/00005Michael J. Fox Foundation for Parkinson's Research, RRIA 2014 Program 10189Ministry of Science, Innovation and Universities (MICIU) (Spain) RYC2022-035429-I
6 · The paper itself

Abstract

objectiveVisual disability in Parkinson's disease (PD) is not fully explained by retinal neurodegeneration. We aimed to delineate the brain substrate of visual dysfunction in PD and its association with retinal thickness.

methodsForty-two PD patients and 29 controls underwent 3-Tesla MRI, retinal spectral-domain optical coherence tomography, and visual testing across four domains. Voxel-level associations between gray matter volume and visual outcomes were used to define a visual impairment region (visualROI). Functional connectivity of the visualROI with brain networks was analyzed. Covariance analysis of brain regions associated with retinal thinning (retinalROI) was conducted using hierarchical clustering to develop a model of retinal and brain neurodegeneration linked to disease progression.

resultsThe amygdala was the primary component of the visualROI, comprising 32.3% and 14.6% of its left and right volumes. Functional connectivity analysis revealed significant disruptions between the visualROI and medial/lateral visual networks in PD. Covariance analysis identified three clusters within retinalROI: (1) the thalamic nucleus, (2) the amygdala and lateral/occipital visual regions, and (3) frontal regions, including the anterior cingulate cortex and frontal attention networks. Hierarchical clustering suggested a two-phase progression: early amygdala damage (Braak 1-3) disrupting visual network connections, followed by retinal and frontal atrophy (Braak 4-5) exacerbating visual dysfunction.

interpretationOur findings support a novel, amygdala-centric two-phase model of visual dysfunction in PD. Early amygdala degeneration disrupts visual pathways, while advanced-stage disconnection between the amygdala and frontal regions and retinal neurodegeneration contributes to further visual disability.

Indexed as

AmygdalaParkinson DiseaseRetinaVision DisordersAgedFemaleGray MatterHumansMagnetic Resonance ImagingMaleMiddle AgedTomography, Optical Coherenceamygdalabrain MRIneurodegenerationretinavision

Identifiers

PMID39957584
PMCPMC12040507

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.