ReviewInternational journal of molecular sciences2021
The PKR/P38/RIPK1 Signaling Pathway as a Therapeutic Target in Alzheimer's Disease.
Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 40 citations in OpenAlex.
- [ModifiedNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- Intranasal Drug Delivery in Neuropharmacology: Advances in Brain-Targeted Therapies and Bioethical Challenges.Biomedicines · 2026Review
- Cerebrospinal fluid markers link to synaptic plasticity responses and Alzheimer's disease genetic pathways.Molecular neurodegeneration · 2025Article
- Identifying and validating immunological biomarkers in obstructive sleep apnea through bioinformatics analysis.Scientific reports · 2025Article
- Insights into targeted ferroptosis in mechanisms, biology, and role of Alzheimer's disease: an update.Frontiers in aging neuroscience · 2025Review
- The relationship mammalian p38 with human health and its homolog Hog1 in response to environmental stresses inFrontiers in cell and developmental biology · 2025Review
- Recent advances in potential enzymes and their therapeutic inhibitors for the treatment of Alzheimer's disease.Heliyon · 2024Review
- Ripks and Neuroinflammation.Molecular neurobiology · 2024Review
- mosGraphGPT: a foundation model for multi-omic signaling graphs using generative AI.bioRxiv : the preprint server for biology · 2024Article
- Epigenome-wide Association Study for Tic Disorders in Children: A Preliminary Study in Korean Population.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2024Article
- Mice with type I interferon signaling deficiency are prone to epilepsy upon HSV-1 infection.Virologica Sinica · 2024Article
- Neurotoxic β-amyloid oligomers cause mitochondrial dysfunction-the trigger for PANoptosis in neurons.Frontiers in aging neuroscience · 2024Review
- PKR downregulation prevents copper-induced synaptic dysfunction and cognitive impairment in a murine model of Wilson's disease.Frontiers in neuroscience · 2024Article
- American Ginseng for the Treatment of Alzheimer's Disease: A Review.Molecules (Basel, Switzerland) · 2023Review
- Discovery and identification of EIF2AK2 as a direct key target of berberine for anti-inflammatory effects.Acta pharmaceutica Sinica. B · 2023Article
- Protein synthesis inhibition and loss of homeostatic functions in astrocytes from an Alzheimer's disease mouse model: a role for ER-mitochondria interaction.Cell death & disease · 2022Article
- DHPA Protects SH-SY5Y Cells from Oxidative Stress-Induced Apoptosis via Mitochondria Apoptosis and the Keap1/Nrf2/HO-1 Signaling Pathway.Antioxidants (Basel, Switzerland) · 2022Article
- The emerging role of autophagy and mitophagy in tauopathies: From pathogenesis to translational implications in Alzheimer's disease.Frontiers in aging neuroscience · 2022Review
- TNF-mediated neuroinflammation is linked to neuronal necroptosis in Alzheimer's disease hippocampus.Acta neuropathologica communications · 2021Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuropathological lesions in Alzheimer's disease (AD) include amyloid plaques formed by the accumulation of amyloid peptides, neurofibrillary tangles made of hyperphosphorylated tau protein, synaptic and neuronal degenerations, and neuroinflammation. The cause of AD is unknown, but according to the amyloid hypothesis, amyloid oligomers could lead to the activation of kinases such as eukaryotic translation initiation factor 2-alpha kinase 2 (PKR), p38, and receptor-interacting serine/threonine-protein kinase 1 (RIPK1), which all belong to the same stress-activated pathway. Many toxic kinase activations have been described in AD patients and in experimental models. A p38 mitogen-activated protein kinase inhibitor was recently tested in clinical trials but with unsuccessful results. The complex PKR/P38/RIPK1 (PKR/dual specificity mitogen-activated protein kinase kinase 6 (MKK6)/P38/MAP kinase-activated protein kinase 2 (MK2)/RIPK1) is highly activated in AD brains and in the brains of AD transgenic animals. To delineate the implication of this pathway in AD, we carried out a search on PubMed including PKR/MKK6/p38/MK2/RIPK1, Alzheimer, and therapeutics. The involvement of this signaling pathway in the genesis of AD lesions, including Aβ accumulations and tau phosphorylation as well as cognitive decline, is demonstrated by the reports described in this review. A future combination strategy with kinase inhibitors should be envisaged to modulate the consequences for neurons and other brain cells linked to the abnormal activation of this pathway.
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