ReviewFrontiers in pharmacology2015
c-Jun N-terminal Kinase (JNK) Signaling as a Therapeutic Target for Alzheimer's Disease.
Review in Frontiers in pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 223 papers, 1 of them a synthesis that pooled it.
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Who cites it
223 citing papers in PubMed, 1 synthesis or guideline pooled it, 412 citations in OpenAlex.
- A Systematic Review of the Biological Effects of Cordycepin.Molecules (Basel, Switzerland) · 2021Pooled it
- Unfolded Protein Response as a Therapeutic Target: 4-(Heptyloxy)phenol Induces Programmed Cell Death in Ewing Sarcoma.Molecular cancer therapeutics · 2026Article
- Article
- Molecular Mechanisms of Neurodegenerative Diseases: Emerging Biomarkers and Therapeutic Targets.Brain sciences · 2026Review
- Features of Alteration in MAPK Pathway Activity in the Postnatal Brain of a Rat Model of Sporadic Alzheimer's Disease.International journal of molecular sciences · 2026Article
- c-Jun in neurodegeneration: A key transcriptional regulator with therapeutic implications.Molecular therapy. Nucleic acids · 2026Review
- Article
- Connecting the Dots: Neurobiological Interplay Between Type 2 Diabetes and Alzheimer's Disease.International journal of molecular sciences · 2026Review
- Attack of the kinases: JNK signaling in metabolism.American journal of physiology. Regulatory, integrative and comparative physiology · 2026Review
- RFWD2 Mitigates AD-Like Cognitive Impairments via the JNK-SGK1 Signaling Pathway in Mice.CNS neuroscience & therapeutics · 2026Article
- TNIK as a molecular switch regulating platelet function in hemostasis and hyperlipidemia-associated thrombosis.Blood advances · 2026Article
- 4-Chlorobenzylamine Containing Maleic Acid Derivatives: Synthesis,ACS chemical neuroscience · 2026Article
- Targeting the JNK Gatekeepers: Structural Evolution and Medicinal Chemistry of MKK4 and MKK7 Inhibitors.Molecules (Basel, Switzerland) · 2026Review
- Targeting tau in Alzheimer's Disease: rationale, approach and challenges.Molecular neurodegeneration · 2026Review
- Metabolites associated with type 2 diabetes and Alzheimer's disease trigger differential intracellular signaling responses in mouse primary neurons.Brain research · 2025Article
- An iPSC-derived neuronal model reveals manganese's role in neuronal endocytosis, calcium flux and mitochondrial bioenergetics.iScience · 2025Article
- Functional Specificity of Astrocyte Subtypes in Alzheimer's Disease: Decoding Disease Mechanisms Through Network-based Analysis of Integrated Single-Nuclei Multi-Omic Data.Molecular neurobiology · 2025Article
- Cell-specific copper dyshomeostasis mechanism in Alzheimer's disease.Translational neurodegeneration · 2025Review
- The Association of Wnt Signaling Pathway Gene Variants, Blood Lipoproteins and Cognitive Function in Elderly People.Molecular neurobiology · 2025Article
- Ferulic acid as a promising candidate for developing selective and effective anti-cancer therapies.Discover oncology · 2025Review
163 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
c-Jun N-terminal kinases (JNKs) are a family of protein kinases that play a central role in stress signaling pathways implicated in gene expression, neuronal plasticity, regeneration, cell death, and regulation of cellular senescence. It has been shown that there is a JNK pathway activation after exposure to different stressing factors, including cytokines, growth factors, oxidative stress, unfolded protein response signals or Aβ peptides. Altogether, JNKs have become a focus of screening strategies searching for new therapeutic approaches to diabetes, cancer or liver diseases. In addition, activation of JNK has been identified as a key element responsible for the regulation of apoptosis signals and therefore, it is critical for pathological cell death associated with neurodegenerative diseases and, among them, with Alzheimer's disease (AD). In addition, in vitro and in vivo studies have reported alterations of JNK pathways potentially associated with pathogenesis and neuronal death in AD. JNK's, particularly JNK3, not only enhance Aβ production, moreover it plays a key role in the maturation and development of neurofibrillary tangles. This review aims to explain the rationale behind testing therapies based on inhibition of JNK signaling for AD in terms of current knowledge about the pathophysiology of the disease. Keeping in mind that JNK3 is specifically expressed in the brain and activated by stress-stimuli, it is possible to hypothesize that inhibition of JNK3 might be considered as a potential target for treating neurodegenerative mechanisms associated with AD.
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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.