Evidence map›Paper›PMID 41254340›Full record

ArticleMolecular neurobiology2025

Proteomic Profiling Reveals Mitochondrial Dysregulation in Rapidly Progressive Alzheimer's: Role of DLDH in Amyloid Beta Aggregation.

Saima Zafar, Aneeqa Noor, Neelam Younas, Mohsin Shafiq, Kathrin Dittmar, Oleksandr Yagensky, Matthias Schmitz, Isidre Ferrer, Peter Hermann, Inga Zerr

Abstract read
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In one paragraph

Article in Molecular neurobiology, 2025. 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

10 authors.

Saima ZafarDepartment of Neurology, Clinical Dementia Centerand, DZNE, Georg-August University, University Medical Center Goettingen (UMG), Robert-Koch-Str. 40, Goettingen, 37075, Germany. saima.zafar@med.uni-goettingen.de.
Aneeqa NoorBiomedical Engineering and Sciences Department, School of Mechanical and Manufacturing Engineering (SMME), National University of Sciences and Technology (NUST), Bolan Road, Islamabad, H-12, 44000, Pakistan.
Neelam YounasDepartment of Neurology, Clinical Dementia Centerand, DZNE, Georg-August University, University Medical Center Goettingen (UMG), Robert-Koch-Str. 40, Goettingen, 37075, Germany.
Mohsin ShafiqDepartment of Neurology, Clinical Dementia Centerand, DZNE, Georg-August University, University Medical Center Goettingen (UMG), Robert-Koch-Str. 40, Goettingen, 37075, Germany.
Kathrin DittmarDepartment of Neurology, Clinical Dementia Centerand, DZNE, Georg-August University, University Medical Center Goettingen (UMG), Robert-Koch-Str. 40, Goettingen, 37075, Germany.
Oleksandr YagenskyDepartment of Neurobiology, Max Planck Institute for Biophysical Chemistry, Goettingen, Germany.
Matthias SchmitzDepartment of Neurology, Clinical Dementia Centerand, DZNE, Georg-August University, University Medical Center Goettingen (UMG), Robert-Koch-Str. 40, Goettingen, 37075, Germany.
Isidre FerrerInstitute of Neuropathology, IDIBELL-University Hospital Bellvitge, University of Barcelona, L'Hospitalet de Llobregat, Barcelona, Spain.
Peter HermannDepartment of Neurology, Clinical Dementia Centerand, DZNE, Georg-August University, University Medical Center Goettingen (UMG), Robert-Koch-Str. 40, Goettingen, 37075, Germany.
Inga ZerrDepartment of Neurology, Clinical Dementia Centerand, DZNE, Georg-August University, University Medical Center Goettingen (UMG), Robert-Koch-Str. 40, Goettingen, 37075, Germany.

Funding

EU Joint Programme - Neurodegenerative Disease Research (JPND) 01ED2407A (PRIONOMICS)International Brain Research Organization Colaborative reserach grant 2023NRPU; Higher Education Commission of Pakistan 15083
6 · The paper itself

Abstract

Alzheimer's disease (AD) is presented as multiple clinical variants depending upon the rate of progression and familial background; however, the exact molecular mechanisms associated with these subtypes and their treatments are yet to be understood. The current study is based on a global proteome analysis of brain samples from patients (n = 38) with rapidly progressive AD (rpAD-survival time < 3 years), sporadic AD (spAD-survival time of 8-10 years), and healthy controls. Proteome analysis revealed a differential regulation of 79 proteins and highlighted the dysregulation of mitochondrial machinery and glucose metabolism in rpAD. Dihydrolipoamide dehydrogenase (DLDH), a mitochondrial oxidoreductase, showed a significant reduction and delocalization in rpAD. In vitro analysis revealed a potential role of DLDH in the aggregation of amyloid beta. Rapid progression in AD may be influenced by the energy homeostasis and redox dysfunction linked with the DLDH.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesDisease ProgressionMitochondriaProtein AggregatesProtein Aggregation, PathologicalProteomicsAgedAged, 80 and overBrainFemaleHumansMaleAmyloid beta-PeptidesProtein AggregatesAlzheimer’s disease (AD)DLDHMetabolic networksMetabolismPost-translational modificationProteomicsRapidly progressive Alzheimer’s disease (rpAD)

Identifiers

PMID41254340
PMCPMC12627125

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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.