ArticleComputational and mathematical methods in medicine2015
Modeling the Interaction between β-Amyloid Aggregates and Choline Acetyltransferase Activity and Its Relation with Cholinergic Dysfunction through Two-Enzyme/Two-Compartment Model.
Article in Computational and mathematical methods in medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 24 citations in OpenAlex.
- Quantitative Systems Pharmacology Development and Application in Neuroscience.Handbook of experimental pharmacology · 2025Review
- Disturbed circadian rhythm and retinal degeneration in a mouse model of Alzheimer's disease.Acta neuropathologica communications · 2023Article
- Hallmarks of neurodegenerative disease: A systems pharmacology perspective.CPT: pharmacometrics & systems pharmacology · 2022Review
- Dissecting Sex-Related Cognition between Alzheimer's Disease and Diabetes: From Molecular Mechanisms to Potential Therapeutic Strategies.Oxidative medicine and cellular longevity · 2021Review
- Influence of hippocampal GABAMetabolic brain disease · 2018Article
- CHAT gene polymorphism rs3810950 is associated with the risk of Alzheimer's disease in the Czech population.Journal of biomedical science · 2018Article
- The influence of two functional genetic variants of GRK5 on tau phosphorylation and their association with Alzheimer's disease risk.Oncotarget · 2017Article
- Epigenetic Treatment of Neurodegenerative Ophthalmic Disorders: An Eye Toward the Future.BioResearch open access · 2017Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The effect of β-amyloid aggregates on activity of choline acetyltransferase (ChAT) which is responsible for synthesizing acetylcholine (ACh) in human brain is investigated through the two-enzyme/two-compartment (2E2C) model where the presynaptic neuron is considered as compartment 1 while both the synaptic cleft and the postsynaptic neuron are considered as compartment 2 through suggesting three different kinetic mechanisms for the inhibition effect. It is found that the incorporation of ChAT inhibition by β-amyloid aggregates into the 2E2C model is able to yield dynamic solutions for concentrations of generated β-amyloid, ACh, choline, acetate, and pH in addition to the rates of ACh synthesis and ACh hydrolysis in compartments 1 and 2. It is observed that ChAT activity needs a high concentration of β-amyloid aggregates production rate. It is found that ChAT activity is reduced significantly when neurons are exposed to high levels of β-amyloid aggregates leading to reduction in levels of ACh which is one of the most significant physiological symptoms of AD. Furthermore, the system of ACh neurocycle is dominated by the oscillatory behavior when ChAT enzyme is completely inhibited by β-amyloid. It is observed that the direct inactivation of ChAT by β-amyloid aggregates may be a probable mechanism contributing to the development of AD.
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