Evidence map›Paper›PMID 42477717›Full record

ArticleActa neuropathologica communications2026

Amygdalar nuclei vulnerability to protein aggregates in Lewy body diseases.

Natasja A C Deshayes, Janna van Wetering, Alex Wesseling, Floris Vos, Angela Ingrassia, Yvon Galis, Laura E Jonkman, Annemieke J M Rozemuller, Wilma D J van de Berg

Abstract read
In one paragraph

Article in Acta neuropathologica communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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

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3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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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

9 authors.

Natasja A C DeshayesSection Clinical Neuroanatomy and Biobanking, Department of Anatomy and Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands. n.a.c.deshayes@amsterdamumc.nl.ORCID https://orcid.org/0009-0002-8602-5075
Janna van WeteringSection Clinical Neuroanatomy and Biobanking, Department of Anatomy and Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands.
Alex WesselingSection Clinical Neuroanatomy and Biobanking, Department of Anatomy and Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands.
Floris VosSection Clinical Neuroanatomy and Biobanking, Department of Anatomy and Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands.
Angela IngrassiaSection Clinical Neuroanatomy and Biobanking, Department of Anatomy and Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands.
Yvon GalisSection Clinical Neuroanatomy and Biobanking, Department of Anatomy and Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands.
Laura E JonkmanSection Clinical Neuroanatomy and Biobanking, Department of Anatomy and Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands.
Annemieke J M RozemullerAmsterdam Neuroscience, Neurodegeneration Program, Amsterdam UMC, Amsterdam, The Netherlands.
Wilma D J van de BergSection Clinical Neuroanatomy and Biobanking, Department of Anatomy and Neurosciences, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam, The Netherlands.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The amygdala is highly vulnerable to protein aggregation and heavily affected in Lewy body diseases (LBDs). However, vulnerability might vary per amygdalar nucleus and it is unclear if the pattern of vulnerability across the nuclei differs between types of protein aggregation and between LBDs. In this study, we aimed to assess the vulnerability of amygdalar nuclei to multiple types of protein aggregation across LBDs. Post-mortem amygdala tissue of donors with incidental LBD (iLBD, n = 6), Parkinson's disease (PD; n = 18), dementia with Lewy bodies (DLB; n = 9) and Alzheimer's disease with Lewy bodies (AD + LB; n = 15) was immunostained with antibodies against alpha-synuclein (aSyn; EP1536Y and 5G4), amyloid beta (Aβ; 4G8), phosphorylated tau (p-tau; AT8) and phosphorylated TDP-43 (p-TDP-43; 11-9), and quantitatively analyzed using QuPath. Neuronal and astrocytic aSyn pathology were most pronounced in the parahippocampal-amygdaloid transition area (PHA) and the basal nucleus, a pattern shared by all disease groups. Vulnerability to Aβ pathology varied per group but was highest in the PHA in AD + LB, whereas diffuse plaques were most common in the accessory basal nucleus. The PHA of DLB and both the basal and accessory basal nucleus of AD + LB cases were most susceptible to p-tau pathology, with fine granular cytoplasmic neuronal tau inclusions being mostly observed in the basal nucleus and neurofibrillary tangles in the accessory basal nucleus. The nuclei in the ventromedial part of the amygdala (PHA, ventral part of the basal nucleus, and cortical nucleus) were found to be hotspots for protein aggregation across LBDs. aSyn pathology in these nuclei predominantly correlated with dementia, hallucinations and anxiety. Our results show that amygdalar nuclei vulnerability differs per protein aggregate and disease entity, although the PHA, basal nucleus and cortical nucleus are generally more vulnerable. Together, our study provides a deeper insight into the selective vulnerability of amygdalar nuclei to protein aggregates and their relation to clinical characteristics in LBDs.

Indexed as

AmygdalaLewy Body DiseaseProtein Aggregation, PathologicalAgedAged, 80 and overalpha-SynucleinAlzheimer DiseaseAmyloid beta-PeptidesDNA-Binding ProteinsFemaleHumansMaleMiddle AgedNeuronsParkinson Diseasetau Proteinsalpha-SynucleinAmyloid beta-PeptidesDNA-Binding ProteinsTARDBP protein, humantau ProteinsAlpha-synucleinAmygdalar nucleiAmyloid betaImmunohistochemistryLewy body diseasePhosphorylated tauVulnerability

Identifiers

PMID42477717
PMCPMC13670467

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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.