Status of Acetylcholinesterase and Butyrylcholinesterase in Alzheimer's Disease and Type 2 Diabetes Mellitus
Open accessAbstract
Both Alzheimer's disease (AD) and Type 2 diabetes mellitus (T2DM) share the presence of systemic and neuro-inflammation, enhanced production and accumulation of β -amyloid peptide and abnormal levels of the enzymes acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE). Altered levels of AChE and BuChE both in AD as well as in T2DM imply that those two enzymes may be playing a pivotal role in the pathogenesis of the two disorders. AD and T2DM are both characterized by elevated levels of AChE and BuChE in the plasma. On the other hand, in AD the brain levels of AChE go down while those of BuChE go up, resulting in deregulation in balance between AChE and BuChE. This imbalance and change in the AChE/BuChE ratio causes cholinergic deficit in the brain, i.e. deficiency in the brain neurotransmitter acetylcholine. With better understanding of the inter-relationship of AChE and BuChE levels in normality as well as abnormality, AD and T2DM can be effectively treated. Thus, general cholinesterase inhibitors that inhibit both AChE and BuChE as well as highly selective BuChE inhibitors may have potential therapeutic benefits in the treatment of AD and other related dementias.
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AChE is typically elevated in Alzheimer's disease patients, especially in the cortex and hippocampus, contributing to cognitive impairment.
“AChE, responsible for the breakdown of ACh, is typically elevated in AD patients, especially in the cortex and hippocampus, contributing to cognitive impairment.”
From Cholinesterase Inhibitors from Plants and Their Potential in Alzheimer’s Treatment: Systematic Review (2025) · cites this paper as [6]
The Introduction says AChE levels fall by as much as 85% in certain brain areas in AD, while BuChE levels rise; it also reports a changed BuChE-to-AChE ratio in cortical areas. The section on targeting these enzymes likewise says AChE activity declines as AD progresses, contrary to the claim that AChE is typically elevated. (LLM, conf=0.91)
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Experimental — accuracy not yet measuredBuChE, although less prominent in healthy brains, increases in Alzheimer's disease, particularly in regions affected by amyloid pathology, potentially compensating for the loss of cholinergic neurons.
“BuChE, although less prominent in healthy brains, increases in AD, particularly in regions affected by amyloid pathology, potentially compensating for the loss of cholinergic neurons [6,7].”
From Cholinesterase Inhibitors from Plants and Their Potential in Alzheimer’s Treatment: Systematic Review (2025) · cites this paper as [6]
The Introduction (page not provided) says BuChE is less abundant than AChE in normal brain and rises as AD progresses. The section on AD pathogenesis links increased BuChE to amyloid plaques and tangles. The paper also describes BuChE’s growing functional importance as AChE declines, but does not say that it compensates for the loss of cholinergic neurons. (LLM, conf=0.86)
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References 85 · Cited by 331
Research works printed but not linked: 3
- [3]Silver A The biology of cholinesterases Elsevier/Agricultural Research Council Institute New York 1974 426 47
- [64]Ali R Sheikh IA Jabir NR Kamal MA Comparative Review of Decade’s Research on Cholinesterase Inhibition Am J Neuroprot Neuroregen 2012 4 1 8
- [87]Greig NH Utsuki T Yu QS Dissociation between the potent β-amyloid protein pathway inhibition and cholinergic actions of the Alzheimer drug candidates phenserine and cymserine Fisher A Memo M Stocchi F Hanin I Advances in Alzheimer’s and Parkinson’s Disease: Insights, Progress, and Perspectives Springer Science + Business Media USA 2008 445 62
- Authors
- Mushtaq, G., Greig, N., Khan, J., & Kamal, M.
- Affiliations
- King Abdulaziz University (SA)
- National Institutes of Health (US)
- Venue
- CNS & Neurological Disorders - Drug Targets
- Publisher
- Bentham Science Publishers Ltd.
- Published
- 2014-11-21
- Volume
- 13
- Issue
- 8
- Pages
- 1432-1439
- ISSN
- 1568-007X (ISSN-L)
- 1871-5273
- PMC
- PMC5878042
- OpenAlex
- W2142587255
- Cited by
- 331
- References
- 85
- Citations by year
- 2026: 31 · 2025: 39 · 2024: 52 · 2023: 43 · 2022: 40 · 2021: 30 · 2020: 30 · 2019: 24 · 2018: 18 · 2017: 13 · 2016: 9 · 2015: 2
- FWCI
- 5.82
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- CNS & Neurological Disorders - Drug Targets (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (Z99 AG999999)
- Topics
- Health Sciences › Medicine › Pharmacology › Cholinesterase and Neurodegenerative Diseases
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Agricultural and Biological Sciences › Plant Science › Pesticide Exposure and Toxicity
- Keywords
- acetylcholinesterase, butyrylcholinesterase, Alzheimer's disease, type 2 diabetes, cholinergic deficit, acetylcholine, amyloid-beta, neuroinflammation, cholinesterase inhibitors, dementia
- MeSH terms
- Acetylcholinesterase, Alzheimer Disease, Animals, Butyrylcholinesterase, Diabetes Mellitus, Type 2, Enzyme Inhibitors, Humans
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