Evidence map›Paper›PMID 42481480›Full record

ArticleNature communications2026

Spatial multi-omics identifies early synaptic pruning and context-specific dopaminergic vulnerability in synucleinopathies.

Svenja-Lotta Rumpf, Felix L Strübing, Karsten Nalbach, Claudia Marina Vargiu, Giacomo Berg, Stefan F Lichtenthaler, Piero Parchi, Pan Gao, Weilin Chen, Matthias Brendel and 6 more

Abstract read
In one paragraph

Article in Nature 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.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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.

Svenja-Lotta Rumpf *German Center for Neurodegenerative Diseases (DZNE), Munich, Germany.
Felix L Strübing *German Center for Neurodegenerative Diseases (DZNE), Munich, Germany.ORCID 0000-0002-9436-6294
Karsten NalbachGerman Center for Neurodegenerative Diseases (DZNE), Munich, Germany.ORCID 0000-0002-3928-4026
Claudia Marina VargiuLaboratorio di Neuropatologia, IRCCS Istituto delle Scienze Neurologiche, Ospedale Bellaria, Bologna, Italy.ORCID 0009-0009-2921-6829
Giacomo BergGerman Center for Neurodegenerative Diseases (DZNE), Munich, Germany.
Stefan F LichtenthalerGerman Center for Neurodegenerative Diseases (DZNE), Munich, Germany.ORCID 0000-0003-2211-2575
Piero ParchiLaboratorio di Neuropatologia, IRCCS Istituto delle Scienze Neurologiche, Ospedale Bellaria, Bologna, Italy.ORCID 0000-0002-9444-9524
Pan GaoGerman Center for Neurodegenerative Diseases (DZNE), Munich, Germany.ORCID 0009-0009-0667-4835
Weilin ChenGerman Center for Neurodegenerative Diseases (DZNE), Munich, Germany.
Matthias BrendelDepartment of Nuclear Medicine, LMU University Hospital, LMU Munich, Munich, Germany.ORCID 0000-0002-9247-2843
Johannes S GnörichGerman Center for Neurodegenerative Diseases (DZNE), Munich, Germany.ORCID 0000-0003-1554-7765
Alexander BernhardtDepartment of Neurology, LMU University Hospital, Ludwig-Maximilians-Universität München, Munich, Germany.ORCID 0000-0002-2572-5062
Léa Dias RodriguesGerman Center for Neurodegenerative Diseases (DZNE), Munich, Germany.
Günter U HöglingerGerman Center for Neurodegenerative Diseases (DZNE), Munich, Germany.ORCID 0000-0001-7587-6187
Jochen HermsGerman Center for Neurodegenerative Diseases (DZNE), Munich, Germany.ORCID 0000-0002-6201-1042
Thomas KoeglspergerGerman Center for Neurodegenerative Diseases (DZNE), Munich, Germany. thomas.koeglsperger@med.uni-muenchen.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parkinson's disease (PD) is characterized by degeneration of dopaminergic neurons in the substantia nigra pars compacta, but the molecular events preceding neuronal loss remain unclear. Here, we combine spatial transcriptomics, spatial proteomics, and α-synuclein (αSyn) seed amplification assays to profile post-mortem midbrain tissue from controls, incidental Lewy body disease (iLBD), PD, Alzheimer's disease (AD), and AD with Lewy body pathology (AD + LBP). We find that αSyn seeding activity correlates with dopaminergic neuron loss in PD-spectrum cases but not in AD-associated LBP, indicating disease-context dependent relationships between αSyn pathology and neurodegeneration. In iLBD, before overt substantia nigra Lewy pathology or detectable αSyn aggregation, we detect increased expression of the complement component C1QC together with loss of inhibitory synaptic markers. These findings support early complement-associated remodeling of inhibitory synapses as a potential pathogenic event preceding overt αSyn aggregation and neuronal degeneration in PD.

Indexed as

Dopaminergic NeuronsNeuronal PlasticityParkinson DiseaseSynucleinopathiesAgedAged, 80 and overalpha-SynucleinAlzheimer DiseaseComplement C1qFemaleHumansLewy Body DiseaseMaleMesencephalonMultiomicsProteomicsalpha-SynucleinComplement C1q

Identifiers

PMID42481480
PMCPMC13392254

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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.