ReviewInternational journal of molecular sciences2021
The Role of Butyrylcholinesterase and Iron in the Regulation of Cholinergic Network and Cognitive Dysfunction in Alzheimer's Disease Pathogenesis.
Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
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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.
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Who cites it
32 citing papers in PubMed, 58 citations in OpenAlex.
- From bench to brain: novel thieno-oxazine hybrids as potent pleiotropic anti-Alzheimer's agents withJournal of enzyme inhibition and medicinal chemistry · 2026Article
- Structure-Based Design of New Series of Sulfonates with Potent and Specific BChE Inhibition and Anti-Inflammatory Effects.International journal of molecular sciences · 2026Article
- Multitargeted Aza-Arylcarboxamides for Neurodegenerative Diseases: Potent Histamine HACS chemical neuroscience · 2026Article
- Mechanistic insights into postoperative delirium using untargeted high-throughput proteomics in elderly patients - a case-control study.Scientific reports · 2026Observational
- Machine Learning-Driven Bioprospecting of Cholinergic Medicinal Plants for Putative Leads Against Butyrylcholinesterase Towards Alzheimer's Care.Biochemistry research international · 2026Article
- Unlocking Therapeutic Potential of Novel Thieno-Oxazepine Hybrids as Multi-Target Inhibitors of AChE/BChE and Evaluation Against Alzheimer's Disease: In Vivo, In Vitro, Histopathological, and Docking Studies.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Multitarget 8-methoxypsoralens against Alzheimer's disease: extraction, synthesis,Future medicinal chemistry · 2025Article
- Serum butyrylcholinesterase activity as a predictor of severity and mortality in COVID-19 patients.Scientific reports · 2025Article
- In silico screening of naturally derived dietary compounds as potential butyrylcholinesterase inhibitors for Alzheimer's disease treatment.Scientific reports · 2025Article
- Synthesis, Biological Evaluation, and Molecular Docking Studies of Novel Coumarin-Triazole-Isatin Hybrids as Selective Butyrylcholinesterase Inhibitors.Molecules (Basel, Switzerland) · 2025Article
- Modulatory Neurotransmitter Genotypes Shape Dynamic Functional Connectome Reconfigurations.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Meroterpenoids from Terrestrial and Marine Fungi: Promising Agents for Neurodegenerative Disorders-An Updated Review.Current issues in molecular biology · 2025Review
- Article
- From Fundamentals to Innovation in Alzheimer's Disease: Molecular Findings and Revolutionary Therapies.International journal of molecular sciences · 2024Review
- Exploring the Benzazoles Derivatives as Pharmacophores for AChE, BACE1, and as Anti-Aβ Aggregation to Find Multitarget Compounds against Alzheimer's Disease.Molecules (Basel, Switzerland) · 2024Review
- Article
- Article
- Review
- Emerging significance of butyrylcholinesterase.World journal of experimental medicine · 2024Review
- Progress of Ferroptosis in Ischemic Stroke and Therapeutic Targets.Cellular and molecular neurobiology · 2024Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Alzheimer's disease (AD), the most common form of dementia in elderly individuals, is marked by progressive neuron loss. Despite more than 100 years of research on AD, there is still no treatment to cure or prevent the disease. High levels of amyloid-β (Aβ) plaques and neurofibrillary tangles (NFTs) in the brain are neuropathological hallmarks of AD. However, based on postmortem analyses, up to 44% of individuals have been shown to have high Aβ deposits with no clinical signs, due to having a "cognitive reserve". The biochemical mechanism explaining the prevention of cognitive impairment in the presence of Aβ plaques is still unknown. It seems that in addition to protein aggregation, neuroinflammatory changes associated with aging are present in AD brains that are correlated with a higher level of brain iron and oxidative stress. It has been shown that iron accumulates around amyloid plaques in AD mouse models and postmortem brain tissues of AD patients. Iron is required for essential brain functions, including oxidative metabolism, myelination, and neurotransmitter synthesis. However, an imbalance in brain iron homeostasis caused by aging underlies many neurodegenerative diseases. It has been proposed that high iron levels trigger an avalanche of events that push the progress of the disease, accelerating cognitive decline. Patients with increased amyloid plaques and iron are highly likely to develop dementia. Our observations indicate that the butyrylcholinesterase (BChE) level seems to be iron-dependent, and reports show that BChE produced by reactive astrocytes can make cognitive functions worse by accelerating the decay of acetylcholine in aging brains. Why, even when there is a genetic risk, do symptoms of the disease appear after many years? Here, we discuss the relationship between genetic factors, age-dependent iron tissue accumulation, and inflammation, focusing on AD.
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Registered trials
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.