ArticleFrontiers in aging neuroscience2022
Coenzyme A-Dependent Tricarboxylic Acid Cycle Enzymes Are Decreased in Alzheimer's Disease Consistent With Cerebral Pantothenate Deficiency.
Article in Frontiers in aging neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 39 citations in OpenAlex.
- Role of B vitamins in modulating homocysteine and metabolic pathways linked to brain atrophy: Metabolomics insights from the VITACOG trial.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Trial
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- Multi-omics integration identifies a gut-microbiota-associated plasma metabolite signature for alzheimer disease diagnosis and metabolic pathway targeting.Frontiers in pharmacology · 2026Article
- Cellular metabolomics reveals the osteogenic mechanism of MC3T3-E1 cells in porous Ti6Al4V scaffolds under low-intensity pulsed ultrasound.Frontiers in cell and developmental biology · 2026Article
- Marine bacteria degrade viral particles as a source of nitrogen, phosphorus, and sulfur-rich dissolved organic matter.ISME communications · 2026Article
- Unveiling Moxibustion's Impact on AD Mice Learning and Memory: Role of Mitochondrial Respiratory Chain Complex I Subunit in the Hippocampus.Molecular neurobiology · 2025Article
- Impairment of Tricarboxylic Acid Cycle (TCA) Cycle in Alzheimer's Disease: Mechanisms, Implications, and Potential Therapies.Aging and disease · 2025Review
- Impact of intraamniotic inflammation on tryptophan metabolism in the placenta-fetal brain axis in rats.Reproduction (Cambridge, England) · 2025Article
- Energy Metabolism and Brain Aging: Strategies to Delay Neuronal Degeneration.Cellular and molecular neurobiology · 2025Review
- Mitochondria and the Repurposing of Diabetes Drugs for Off-Label Health Benefits.International journal of molecular sciences · 2025Review
- Synergistic effects of surface-enhanced Raman spectroscopy and enzyme-linked immunoassays in diagnosis of Alzheimer's disease, mild cognitive impairment, and late-life depression.Frontiers in neurology · 2025Article
- Development of a Novel Mitochondrial Dysfunction-Related Alzheimer's Disease Diagnostic Model Using Bioinformatics and Machine Learning.Current Alzheimer research · 2025Article
- Say hello to my little friend… micronutraceuticals in neuroenergetics, neuronal health, and neurodegenerative diseases.Frontiers in neuroscience · 2025Review
- Altered metabolic function induced by Aβ-oligomers and PSEN1 mutations in iPSC-derived astrocytes.Journal of neurochemistry · 2025Article
- Impact of aNutrients · 2024Article
- Localized Pantothenic Acid (Vitamin B5) Reductions Present Throughout the Dementia with Lewy Bodies Brain.Journal of Parkinson's disease · 2024Article
- Bioinorganic Chemistry of Micronutrients Related to Alzheimer's and Parkinson's Diseases.Molecules (Basel, Switzerland) · 2023Review
- A Targeted Mass Spectrometry Approach to Identify Peripheral Changes in Metabolic Pathways of Patients with Alzheimer's Disease.International journal of molecular sciences · 2023Article
- Integrated multi-omics analysis of Alzheimer's disease shows molecular signatures associated with disease progression and potential therapeutic targets.Scientific reports · 2023Article
- Tissue-Specific Sex Difference in Mouse Eye and Brain Metabolome Under Fed and Fasted States.Investigative ophthalmology & visual science · 2023Article
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
Sporadic Alzheimer's disease (sAD) is the commonest cause of age-related neurodegeneration and dementia globally, and a leading cause of premature disability and death. To date, the quest for a disease-modifying therapy for sAD has failed, probably reflecting our incomplete understanding of aetiology and pathogenesis. Drugs that target aggregated Aβ/tau are ineffective, and metabolic defects are now considered to play substantive roles in sAD pathobiology. We tested the hypothesis that the recently identified, pervasive cerebral deficiency of pantothenate (vitamin B5) in sAD, might undermine brain energy metabolism by impairing levels of tricarboxylic acid (TCA)-cycle enzymes and enzyme complexes, some of which require the pantothenate-derived cofactor, coenzyme A (CoA) for their normal functioning. We applied proteomics to measure levels of the multi-subunit TCA-cycle enzymes and their cytoplasmic homologues. We analysed six functionally distinct brain regions from nine sAD cases and nine controls, measuring 33 cerebral proteins that comprise the nine enzymes of the mitochondrial-TCA cycle. Remarkably, we found widespread perturbations affecting only two multi-subunit enzymes and two enzyme complexes, whose function is modulated, directly or indirectly by CoA: pyruvate dehydrogenase complex, isocitrate dehydrogenase, 2-oxoglutarate dehydrogenase complex, and succinyl-CoA synthetase. The sAD cases we studied here displayed widespread deficiency of pantothenate, the obligatory precursor of CoA. Therefore, deficient cerebral pantothenate can damage brain-energy metabolism in sAD, at least in part through impairing levels of these four mitochondrial-TCA-cycle enzymes.
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Registered trials
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