Evidence map›Paper›PMID 39711511›Full record

ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2025

Proteomic signatures of Alzheimer's disease and Lewy body dementias: A comparative analysis.

Anna Canal-Garcia, Rui M Branca, Paul T Francis, Clive Ballard, Bengt Winblad, Janne Lehtiö, Per Nilsson, Dag Aarsland, Joana B Pereira, Erika Bereczki

Abstract readComparative Study
In one paragraph

Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed.

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  14. Proteomic signatures of Alzheimer's disease and Lewy body dementias: A comparative analysis.Alzheimer's & dementia : the journal of the Alzheimer's Association · 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

10 authors.

Anna Canal-GarciaDepartment of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
Rui M BrancaDepartment of Oncology-Pathology, Science for Life Laboratory, Karolinska Institutet, Stockholm, Sweden.
Paul T FrancisKing's College London, Wolfson Centre for Age-Related Diseases, London, UK.
Clive BallardUniversity of Exeter Medical School, University of Exeter, Exeter, UK.
Bengt WinbladDepartment of Neurobiology, Care Sciences and Society, Center for Alzheimer Research, Division of Neurogeriatrics, Karolinska Institutet, BioClinicum, Stockholm, Sweden.
Janne LehtiöDepartment of Oncology-Pathology, Science for Life Laboratory, Karolinska Institutet, Stockholm, Sweden.
Per NilssonDepartment of Neurobiology, Care Sciences and Society, Center for Alzheimer Research, Division of Neurogeriatrics, Karolinska Institutet, BioClinicum, Stockholm, Sweden.
Dag AarslandDepartment of Neurobiology, Care Sciences and Society, Center for Alzheimer Research, Division of Neurogeriatrics, Karolinska Institutet, BioClinicum, Stockholm, Sweden.
Joana B PereiraDepartment of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
Erika BereczkiDepartment of Neurobiology, Care Sciences and Society, Center for Alzheimer Research, Division of Neurogeriatrics, Karolinska Institutet, BioClinicum, Stockholm, Sweden.ORCID 0000-0002-0373-7417

Funding

DemensfondenDemensfonden, Gamla Tjanarinnor Foundation, Stohnes Stiftelse, Loo och Hans Osterman Foundation, Magnus Berwall Foundation, Längmanska kulturfonden,Gun och Bertil Stohnes StiftelseLindhes Advokatbyra foundationLoo och Hans Ostermans Stiftelse för Medicinsk ForskningMagnus Bergvalls StiftelseStiftelsen för Gamla TjänarinnorStiftelsen Längmanska Kulturfonden
6 · The paper itself

Abstract

introductionWe aimed to identify unique proteomic signatures of Alzheimer's disease (AD), dementia with Lewy bodies (DLB), and Parkinson's disease dementia (PDD).

methodsWe conducted a comparative proteomic analysis of 33 post mortem brains from AD, DLB, and PDD individuals without dementia focusing on prefrontal, cingulate, and parietal cortices, using weighted gene co-expression network analyses with differential enrichment analysis.

resultsNetwork modules revealed hub proteins common to all dementias. Lewy body dementias differed from AD by reduced levels of the autophagy protein p62 (SQSTM1), whereas DLB was distinguished from both AD and PDD by altered TRIM33 and cysteine/glutamate transporter (SLC7A11) across brain regions. An increase in mitochondrial and synaptic proteins was related to better cognition whereas enrichment in the extracellular matrix, complement system, and autophagy proteins was associated with greater cognitive impairment. DISCUSSION: Our study offers valuable insights into the network-based biomarker characterization of molecular signatures of AD, DLB, and PDD. HIGHLIGHTS: Reduced levels of the autophagy protein p62 (SQSTM1) differentiated Lewy body dementias from Alzheimer's disease (AD) across multiple brain regions. Dementia with Lewy bodies (DLB) was distinguished from both AD and Parkinson's disease dementia (PDD) by altered TRIM33 and cysteine/glutamate transporter (SLC7A11) levels across brain regions. Key mitochondrial oxidative phosphorylation proteins (e.g., COX7A2, TOMM40L, NDUFV1), and synaptic proteins (e.g., GABRB3, GABRB2, GLUA3, GLUA4, SNAP47, dynamin1) were more abundant in preserved cognitive states. Extracellular matrix proteins and members of the complement system (decorin, biglycan, C4A, C4B) showed a strong positive correlation with cognitive decline.

Indexed as

Alzheimer DiseaseBrainLewy Body DiseaseProteomicsAgedAged, 80 and overBiomarkersFemaleHumansMaleParkinson DiseaseSequestosome-1 ProteinBiomarkersSequestosome-1 ProteinSQSTM1 protein, humanAlzheimer's diseaseco‐expression network analysiscognitive impairmentLewy body dementiasmass spectrometrysynaptic proteins

Identifiers

PMID39711511
PMCPMC11780320

What OpenQuestion holds

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LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.