ArticleBrain sciences2022
Computational Analysis of Pathogenetic Pathways in Alzheimer's Disease and Prediction of Potential Therapeutic Drugs.
Article in Brain sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 6 citations in OpenAlex.
- Advancing Alzheimer's Therapy: Computational strategies and treatment innovations.IBRO neuroscience reports · 2025Review
- Cross-Species Modeling Identifies Gene Signatures in Type 2 Diabetes Mouse Models Predictive of Inflammatory and Estrogen Signaling Pathways Associated with Alzheimer's Disease Outcomes in Humans.Pacific Symposium on Biocomputing. Pacific Symposium on Biocomputing · 2025Article
- In-vivo neuronal dysfunction by Aβ and tau overlaps with brain-wide inflammatory mechanisms in Alzheimer's disease.Frontiers in aging neuroscience · 2024Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAlzheimer's disease (AD) is a chronic and progressive neurodegenerative disease which affects more than 50 million patients and represents 60-80% of all cases of dementia. Mutations in the APP gene, mostly affecting the γ-secretase site of cleavage and presenilin mutations, have been identified in inherited forms of AD.
methodsIn the present study, we performed a meta-analysis of the transcriptional signatures that characterize two familial AD mutations (APP
resultsOverall, the meta-analysis identified 1479 differentially expressed genes (DEGs), 684 downregulated genes, and 795 upregulated genes. Additionally, we found 14 drugs with a significant anti-similarity to the AD signature, with the top five drugs being naftifine, moricizine, ketoconazole, perindopril, and fexofenadine.
conclusionsThis study aimed to integrate the transcriptional profiles associated with common familial AD mutations in neurons in order to characterize the pathogenetic mechanisms involved in AD and to find more effective drugs for AD.
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