ArticleThe open neurology journal2009
Pharmacological Treatment of Alzheimer's Disease: Is it Progressing Adequately?
Article in The open neurology journal, 2009. 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
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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.
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.
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Who cites it
4 citing papers in PubMed.
- Two-Dimensional MXene-Loaded Butylphthalide Enhances the Treatment of Alzheimer's Disease by Inhibiting Ferroptosis and Oxidative Stress.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Resveratrol as a Therapeutic Agent in Alzheimer's Disease: Evidence from Clinical Studies.Nutrients · 2025Review
- Current biomarkers and treatment strategies in Alzheimer disease: An overview and future perspectives.IBRO neuroscience reports · 2024Review
- Beyond the cholinergic hypothesis: do current drugs work in Alzheimer's disease?CNS neuroscience & therapeutics · 2010Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionBetween 1993 and 2000 four acetylcholinesterase inhibitors were marketed as a symptomatic treatment for Alzheimer's disease (AD), as well as memantine in 2003. Current research is focused on finding drugs that favorably modify the course of the disease. However, their entrance into the market does not seem to be imminent. RESEARCH DEVELOPMENT: The aim of AD research is to find substances that inhibit certain elements of the AD pathogenic chain (beta- and gamma-secretase inhibitors, alpha-secretase stimulants, beta-amyloid aggregability reducers or disaggregation and elimination inductors, as well as tau-hyperphosphorylation, glutamate excitotoxicity, oxidative stress and mitochondrial damage reducers, among other action mechanisms). Demonstrating a disease's retarding effect demands longer trials than those necessary to ascertain symptomatic improvement. Besides, a high number of patients (thousands of them) is necessary, all of which turns out to be difficult and costly. Furthermore, it would be necessary to count on diagnosis and progression markers in the disease's pre-clinical stage, markers for specific phenotypes, as well as high-selectivity molecules acting only where necessary. In order to compensate these difficulties, drugs acting on several defects of the pathogenic chain or showing both symptomatic and neuroprotective action simultaneously are being researched.
conclusionsThere are multiple molecules used in research to modify AD progression. Although it turns out to be difficult to obtain drugs with sufficient efficacy so that their marketing is approved, if they were achieved they would lead to a reduction of AD prevalence.
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Registered trials
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