ArticleJournal of molecular neuroscience : MN2014
Acetylcholinesterase protein level is preserved in the Alzheimer's brain.
Article in Journal of molecular neuroscience : MN, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 25 citations in OpenAlex.
- An investigation into the use of Caenorhabditis elegans as a model organism for nerve agent exposure research.Neurotoxicology · 2026Article
- Low-Dimensional Nanomaterials in Alzheimer's Disease: Current Applications.Current Alzheimer research · 2026Review
- Evidence for a novel neuronal mechanism driving Alzheimer's disease, upstream of amyloid.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Review
- Evaluation of the Neuroprotective Effect of Organic Selenium Compounds: An in Vitro Model of Alzheimer's Disease.Biological trace element research · 2024Article
- Identification of a Novel Wnt Antagonist Based Therapeutic and Diagnostic Target for Alzheimer's Disease Using a Stem Cell-Derived Model.Bioengineering (Basel, Switzerland) · 2023Article
- Presenilin 1 Modulates Acetylcholinesterase Trafficking and Maturation.International journal of molecular sciences · 2023Article
- Proceedings of workshop: "Neuroglycoproteins in health and disease", INNOGLY cost action.Glycoconjugate journal · 2022Article
- Synergistic Inhibition of Acetylcholinesterase by Alkaloids Derived from Stephaniae Tetrandrae Radix, Coptidis Rhizoma and Phellodendri Chinensis Cortex.Molecules (Basel, Switzerland) · 2019Article
- Early growth response-1 regulates acetylcholinesterase and its relation with the course of Alzheimer's disease.Brain pathology (Zurich, Switzerland) · 2019Article
- Hydrogen peroxide modifies both activity and isoforms of acetylcholinesterase in human neuroblastoma SH-SY5Y cells.Redox biology · 2017Article
- Biogenesis, assembly and trafficking of acetylcholinesterase.Journal of neurochemistry · 2017Review
- Increased Expression of Readthrough Acetylcholinesterase Variants in the Brains of Alzheimer's Disease Patients.Journal of Alzheimer's disease : JAD · 2016Article
- Satureja bachtiarica ameliorate beta-amyloid induced memory impairment, oxidative stress and cholinergic deficit in animal model of Alzheimer's disease.Metabolic brain disease · 2016Article
- Rescue and Stabilization of Acetylcholinesterase in Skeletal Muscle by N-terminal Peptides Derived from the Noncatalytic Subunits.The Journal of biological chemistry · 2015Article
- Journal of molecular neuroscience: impacting our brains.Journal of molecular neuroscience : MN · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acetylcholinesterase (AChE) is a key enzyme in the cholinergic nervous system and is one of the most studied proteins in the field of Alzheimer's disease (AD). Moreover, alternative functions of AChE unrelated with the hydrolysis of acetylcholine are suspected. Until now, the majority of investigations on AChE in AD pathology have been focused on the determination of its enzymatic activity level, which is depleted in the AD brain. Despite this overall decrease, AChE activity increases at the vicinity of the two hallmarks of AD, the amyloid plaques and the neurofibrillary tangles (NFT). In fact, AChE may directly interact with Aβ in a manner that increases the deposition of Aβ to form plaques. In the context of protein-protein interactions, we have recently reported that AChE can interact with presenilin-1, the catalytic component of γ-secretase, influencing its expression level and also its activity. However, the alteration of AChE protein in the AD brain has not been determined. Here, we demonstrated by Western blotting and immunohistochemistry that a prominent pool of enzymatically inactive AChE protein existed in the AD brain. The potential significance of these unexpected levels of inactive AChE protein in the AD brain was discussed, especially in the context of protein-protein interactions with β-amyloid and presenilin-1.
Indexed as
Identifiers
What OpenQuestion holds
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.