ReviewHeliyon2024
Recent advances in potential enzymes and their therapeutic inhibitors for the treatment of Alzheimer's disease.
Review in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed.
- Biological activity of Pleurotus eryngii based on antioxidant, anticholinesterase and antiproliferative effects using optimized extraction methods.Scientific reports · 2026Article
- Review
- Development of coumarin-sulfonate scaffolds for cholinesterase inhibition: experimental and computational studies toward Alzheimer's disease therapy.RSC advances · 2026Article
- Histone Deacetylase 2 in Alzheimer's Disease: A Comprehensive Molecular Blueprint for Therapeutic Targeting.Molecular neurobiology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD), a chronic neurodegenerative disease, is clinically characterized by loss of memory and learning ability among other neurological deficits. Amyloid plaques, hyperphosphorylated tau protein, and neurofibrillary tangles involve in AD etiology. Meanwhile, enzymes and their inhibitors have become the focus of research in AD treatment. In this review, the molecular mechanisms involved in the pathogenesis of AD were overviewed and various enzymes such as acetylcholinesterase (AChE), butyrylcholinesterase (BuChE), β-secretase, γ-secretase, monoamine oxidase (MAO), and receptor of advanced glycation end products (RAGE) were highlighted as potential targets for AD treatment. Several hybrid molecules with essential substructures derived from various chemotypes have demonstrated desired pharmacological activity. It is envisioned that the development of new drugs that inhibit enzymes involved in AD is a future trend in the management of the disease.
Indexed as
Identifiers
What Socratic 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 Socratic graph.