ReviewPharmaceuticals (Basel, Switzerland)2024
Investigation of Potential Drug Targets Involved in Inflammation Contributing to Alzheimer's Disease Progression.
Review in Pharmaceuticals (Basel, Switzerland), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Altered tear fluid protein expression in persons with mild cognitive impairment.Journal of Alzheimer's disease : JAD · 2026Article
- Targeting protein kinase C signaling cascades in alzheimer's disease: emerging neuroprotective roles of aurothioglucose.Inflammopharmacology · 2026Review
- Induced Microglial-like Cells Derived from Familial and Sporadic Alzheimer's Disease Peripheral Blood Monocytes Show Abnormal Phagocytosis and Inflammatory Response to PSEN1 E280A Cholinergic-like Neurons.International journal of molecular sciences · 2025Article
- Mini meta-analysis of anticholinesterase actions of atorvastatin, simvastatin and rosuvastatin, andToxicology reports · 2025Review
- New and potential boron-containing compounds for treatment of Alzheimer's disease and cancers.Future medicinal chemistry · 2025Article
- VEXAS Syndrome and Alzheimer's Disease-Are There Connections?Brain sciences · 2025Review
- Anti-inflammatory effects ofScientific reports · 2025Article
- Gene Co-Expression Analysis Reveals Functional Differences Between Early- and Late-Onset Alzheimer's Disease.Current issues in molecular biology · 2025Article
- Unveiling the Interplay: Neurovascular Coupling, Astrocytes and G Protein-Coupled Receptors in Alzheimer's Disease.ACS pharmacology & translational science · 2025Review
- Repurposing FDA-Approved Drugs Against Potential Drug Targets Involved in Brain Inflammation Contributing to Alzheimer's Disease.Targets (Basel) · 2024Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease has become a major public health issue. While extensive research has been conducted in the last few decades, few drugs have been approved by the FDA to treat Alzheimer's disease. There is still an urgent need for understanding the disease pathogenesis, as well as identifying new drug targets for further drug discovery. Alzheimer's disease is known to arise from a build-up of amyloid beta (Aβ) plaques as well as tangles of tau proteins. Along similar lines to Alzheimer's disease, inflammation in the brain is known to stem from the degeneration of tissue and build-up of insoluble materials. A minireview was conducted in this work assessing the genes, proteins, reactions, and pathways that link brain inflammation and Alzheimer's disease. Existing tools in Systems Biology were implemented to build protein interaction networks, mainly for the classical complement pathway and G protein-coupled receptors (GPCRs), to rank the protein targets according to their interactions. The top 10 protein targets were mainly from the classical complement pathway. With the consideration of existing clinical trials and crystal structures, proteins C5AR1 and GARBG1 were identified as the best targets for further drug discovery, through computational approaches like ligand-protein docking techniques.
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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.