ArticleCells2019
Genetic and Real-World Clinical Data, Combined with Empirical Validation, Nominate Jak-Stat Signaling as a Target for Alzheimer's Disease Therapeutic Development.
Article in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 51 citations in OpenAlex.
- Computational Repurposing of Janus Kinase Inhibitors as Potential Therapeutic Candidates for Alzheimer's Disease.Medicina (Kaunas, Lithuania) · 2026Article
- Pharmacological targeting of the JAK-STAT pathway: new concepts and emerging indications.Nature reviews. Drug discovery · 2026Review
- TYK2 mediates neuroinflammation in Alzheimer's disease brains with TDP-43 pathology.Nature communications · 2026Article
- Deciphering the Multi-Target Therapeutic Mechanisms of Traditional Chinese Medicine Against Alzheimer's Disease: A Network Pharmacology Perspective.Drug design, development and therapy · 2026Review
- The evolution of Alzheimer's target identification: Towards a fusion of artificial and cellular intelligence.The journal of prevention of Alzheimer's disease · 2025Article
- Exploring bacterial metabolites in microbe-human host dialogue and their therapeutic potential in Alzheimer's diseases.Molecular diversity · 2025Article
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- Targeting the JAK/STAT3/SOCS signaling pathway in Alzheimer's disease.Inflammopharmacology · 2025Review
- Amyloid beta-induced signalling in leptomeningeal cells and its impact on astrocyte response.Molecular and cellular biochemistry · 2025Article
- Identification and Exploration of Immunity-Related Genes and Natural Products for Alzheimer's Disease Based on Bioinformatics, Molecular Docking, and Molecular Dynamics.Immunity, inflammation and disease · 2025Article
- Modulating Neuroinflammation as a Prospective Therapeutic Target in Alzheimer's Disease.Cells · 2025Review
- Molecular Mechanisms Underlying Neuroinflammation Intervention with Medicinal Plants: A Critical and Narrative Review of the Current Literature.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Intranasal administration ofFrontiers in pharmacology · 2025Article
- Characterization of gene expression profiles in Alzheimer's disease and osteoarthritis: A bioinformatics study.PloS one · 2025Article
- Identification of Plasma Cell Subsets and Molecular Markers of Alzheimer's Disease Based on Single-Cell Weighted Gene Co-Expression Network Analysis, Mendelian Randomization Analysis and Clinical Validation.International journal of general medicine · 2025Article
- Diverse signaling mechanisms and heterogeneity of astrocyte reactivity in Alzheimer's disease.Journal of neurochemistry · 2024Review
- TYK2 as a novel therapeutic target in Alzheimer's Disease with TDP-43 inclusions.bioRxiv : the preprint server for biology · 2024Article
- Signalling Pathways Involved in Microglial Activation in Alzheimer's Disease and Potential Neuroprotective Role of Phytoconstituents.CNS & neurological disorders drug targets · 2024Review
- Qi Fu Yin ameliorates neuroinflammation through inhibiting RAGE and TLR4/NF-κB pathway in AD model rats.Aging · 2023Article
Corrections and comments
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Authors and funding
10 authors at 6 institutions in 3 countries.
Funding
Abstract
As genome-wide association studies (GWAS) have grown in size, the number of genetic variants that have been associated per disease has correspondingly increased. Despite this increase in the number of single-nucleotide polymorphisms (SNPs) identified per disease, their biological interpretation has in many cases remained elusive. To address this, we have combined GWAS results with orthogonal sources of evidence, namely the current knowledge of molecular pathways; real-world clinical data from six million patients; RNA expression across tissues from Alzheimer's disease (AD) patients, and purpose-built rodent models for experimental validation. In more detail, first we show that when examined at a pathway level, analysis of all GWAS studies groups AD in a cluster with disorders of immunity and inflammation. Using clinical data, we show that the degree of comorbidity of these diseases with AD correlates with the strength of their genetic association with molecular participants in the Janus kinases/signal transducer and activator of transcription (JAK-STAT) pathway. Using four independent RNA expression datasets we then find evidence for the altered regulation of JAK-STAT pathway genes in AD. Finally, we use both in vitro and in vivo rodent models to demonstrate that Aβ induces gene expression of the key drivers of this pathway, providing experimental evidence to validate these data-driven observations. These results therefore nominate JAK-STAT anomalies as a prominent aetiopathological event in AD and hence a potential target for therapeutic development, and moreover demonstrate a de novo multi-modal approach to derive information from rapidly increasing genomic datasets.
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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.