Evidence mapPaperPMID 41945181Full record

ReviewMetabolic brain disease2026

The role of 2-Oxoglutarate dehydrogenase complex mitochondrial enzyme in alzheimer's disease: a literature review and bioinformatics workflow.

Fatemeh Sayehmiri, Mohanna Parvenous, Kimia Vakili, Rasoul Ebrahimi, Zehra Batool, Narges Bazgir, Kiarash Kazemi, Maral Moafi, Mohammad Javad Ebrahimi, Mohammadreza Hajiesmaeili

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In one paragraph

Review in Metabolic brain disease, 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

10 authors.

Fatemeh Sayehmiri *Skull Base Research Center, Loghman Hakim Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran.ORCID http://orcid.org/0000-0003-3361-2786
Mohanna Parvenous *School of Medicine, Iran University of Medical Sciences, Tehran, Iran.ORCID http://orcid.org/0009-0006-2845-2078
Kimia VakiliStudent Research Committee, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.ORCID http://orcid.org/0000-0001-7296-3218
Rasoul EbrahimiSchool of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.ORCID http://orcid.org/0009-0004-0991-7752
Zehra BatoolDr. Panjwani Center for Molecular Medicine and Drug Research, International Center for Chemical and Biological Sciences, University of Karachi, Karachi, Pakistan.ORCID http://orcid.org/0000-0002-9593-9306
Narges BazgirHearing Disorders Research Center, Loghman Hakim Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran.ORCID http://orcid.org/0000-0002-6443-9448
Kiarash KazemiSchool of Medicine, Tehran University of Medical Sciences, Tehran, Iran.ORCID http://orcid.org/0000-0002-3515-7118
Maral MoafiCell Biology and Anatomical Sciences, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.ORCID http://orcid.org/0000-0002-4099-4017
Mohammad Javad EbrahimiCell Biology and Anatomical Sciences, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. Ebrahimi137377@gmail.com.ORCID http://orcid.org/0000-0002-9440-7340
Mohammadreza HajiesmaeiliCritical Care Quality Improvement Research Center, Loghman Hakim Hospital, Shahid Beheshti University of Medical Sciences, Box. 19839-6311, Tehran, Iran. hajiesmaeilimohammadreza@gmail.com.ORCID http://orcid.org/0000-0003-0023-810X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer’s disease (AD) is a leading neurodegenerative disorder and a significant cause of senile dementia. While the exact mechanisms of AD remain unclear, key hypotheses include the accumulation of amyloid-β (Aβ) plaques and hyperphosphorylated Tau tangles in the hippocampus and cortex. Recent evidence highlights the significant role of damaged mitochondria in AD pathogenesis. Abnormal glucose metabolism contributes to neurodegeneration by affecting enzymes in the tricarboxylic acid (TCA) cycle, particularly the mitochondrial 2-oxoglutarate dehydrogenase (OGDHC) complex, which is vital for the oxidative decarboxylation of 2-oxoglutarate. Impaired OGDHC function is associated with energy failure, oxidative stress, neuroinflammation, and calcium irregularities, all of which may worsen AD progression. This study reviews the evidence linking mitochondrial dysfunction to AD, emphasizing OGDHC deficiency. Additionally, we conducted a bioinformatics analysis to identify key genes in mitochondrial metabolic pathways, highlighting the critical role of OGDHC in AD-related mitochondrial dysfunction (Graphical abstract = Fig. 2).

Indexed as

Alzheimer DiseaseComputational BiologyKetoglutarate Dehydrogenase ComplexMitochondriaAnimalsCitric Acid CycleHumansOxidative StressKetoglutarate Dehydrogenase Complex2-oxoglutarate dehydrogenaseAlzheimer’s diseaseOGDHCTricarboxylic acid cycle

Identifiers

What Socratic holds

Textmetadata
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 Socratic graph.