ReviewNeurochemical research2013
Acetyl-CoA the key factor for survival or death of cholinergic neurons in course of neurodegenerative diseases.
Review in Neurochemical research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.
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Who cites it
52 citing papers in PubMed, 1 synthesis or guideline pooled it, 112 citations in OpenAlex.
- Evaluation of Metabolic and Synaptic Dysfunction Hypotheses of Alzheimer's Disease (AD): A Meta-Analysis of CSF Markers.Current Alzheimer research · 2018Pooled it
- N-Acetylaspartate Synthesis as a Thermodynamic Relief Mechanism for Mitochondrial Aspartate Aminotransferase.bioRxiv : the preprint server for biology · 2026Article
- Differential Effects of Hypoglycemia and Excitotoxic Signals on SN56 Septal Cholinergic Neuronal Cells.Cells · 2026Article
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- Pathological Sequelae of Chronic Vestibular Migraine and Cerebrovascular Insufficiency Leading to Cognitive Decline and Dementia.Indian journal of otolaryngology and head and neck surgery : official publication of the Association of Otolaryngologists of India · 2025Article
- Bioinformatics-driven untargeted metabolomic profiling for clinical screening of methamphetamine abuse.Forensic toxicology · 2025Article
- Thiamine, gastrointestinal beriberi and acetylcholine signaling.Frontiers in nutrition · 2025Review
- The looming threat of profenofos organophosphate and microbes in action for their sustainable degradation.Environmental science and pollution research international · 2024Review
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- STZ-induced hyperglycemia differentially influences mitochondrial distribution and morphology in the habenulointerpeduncular circuit.Frontiers in cellular neuroscience · 2024Article
- Effects of Marginal Zn Excess and Thiamine Deficiency on Microglial N9 Cell Metabolism and Their Interactions with Septal SN56 Cholinergic Cells.International journal of molecular sciences · 2023Article
- Evaluation of eGFP expression in the ChAT-eGFP transgenic mouse brain.BMC neuroscience · 2023Article
- The Novel Role of Mitochondrial Citrate Synthase and Citrate in the Pathophysiology of Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2023Review
- Motor and somatosensory degenerative myelopathy responsive to pantothenic acid in piglets.Veterinary pathology · 2023Article
- Altered energy metabolism in Fatal Familial Insomnia cerebral organoids is associated with astrogliosis and neuronal dysfunction.PLoS genetics · 2023Article
- Metabolic and Cellular Compartments of Acetyl-CoA in the Healthy and Diseased Brain.International journal of molecular sciences · 2022Review
- Coenzyme A-Dependent Tricarboxylic Acid Cycle Enzymes Are Decreased in Alzheimer's Disease Consistent With Cerebral Pantothenate Deficiency.Frontiers in aging neuroscience · 2022Article
- Protection of Cholinergic Neurons against Zinc Toxicity by Glial Cells in Thiamine-Deficient Media.International journal of molecular sciences · 2021Article
- Branched-chain amino acids govern the high learning ability phenotype in Tokai high avoider (THA) rats.Scientific reports · 2021Article
- Role of Energy Metabolism in the Progression of Neuroblastoma.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glucose-derived pyruvate is a principal source of acetyl-CoA in all brain cells, through pyruvate dehydogenase complex (PDHC) reaction. Cholinergic neurons like neurons of other transmitter systems and glial cells, utilize acetyl-CoA for energy production in mitochondria and diverse synthetic pathways in their extramitochondrial compartments. However, cholinergic neurons require additional amounts of acetyl-CoA for acetylcholine synthesis in their cytoplasmic compartment to maintain their transmitter functions. Characteristic feature of several neurodegenerating diseases including Alzheimer's disease and thiamine diphosphate deficiency encephalopathy is the decrease of PDHC activity correlating with cholinergic deficits and losses of cognitive functions. Such conditions generate acetyl-CoA deficits that are deeper in cholinergic neurons than in noncholinergic neuronal and glial cells, due to its additional consumption in the transmitter synthesis. Therefore, any neuropathologic conditions are likely to be more harmful for the cholinergic neurons than for noncholinergic ones. For this reason attempts preserving proper supply of acetyl-CoA in the diseased brain, should attenuate high susceptibility of cholinergic neurons to diverse neurodegenerative conditions. This review describes how common neurodegenerative signals could induce deficts in cholinergic neurotransmission through suppression of acetyl-CoA metabolism in the cholinergic neurons.
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