ReviewFrontiers in aging neuroscience2014
Cyclin-dependent kinase 5, a node protein in diminished tauopathy: a systems biology approach.
Review in Frontiers in aging neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- Tau physiology and pathology: impacts on cellular structures and neurodegenerative diseases.Inflammopharmacology · 2026Review
- Multi-target approach to Alzheimer's disease prevention and treatment: antioxidant, anti-inflammatory, and amyloid- modulating mechanisms.Neurogenetics · 2025Review
- Role of Nanoparticle-Conjugates and Nanotheranostics in Abrogating Oxidative Stress and Ameliorating Neuroinflammation.Antioxidants (Basel, Switzerland) · 2023Review
- Deficiency of Parkinson's Related Protein DJ-1 Alters Cdk5 Signalling and Induces Neuronal Death by Aberrant Cell Cycle Re-entry.Cellular and molecular neurobiology · 2023Article
- Neurodegeneration and convergent factors contributing to the deterioration of the cytoskeleton in Alzheimer's disease, cerebral ischemia and multiple sclerosis (Review).Biomedical reports · 2022Review
- Delivery of Intravenously Administered Antibodies Targeting Alzheimer's Disease-Relevant Tau Species into the Brain Based on Receptor-Mediated Transcytosis.Pharmaceutics · 2022Review
- A Novel NMDA Receptor Antagonist Protects against Cognitive Decline Presented by Senescent Mice.Pharmaceutics · 2020Article
- Regulation of in vivo dynein force production by CDK5 and 14-3-3ε and KIAA0528.Nature communications · 2019Article
- Frontotemporal Lobar Degeneration: Mechanisms and Therapeutic Strategies.Molecular neurobiology · 2016Review
- Selenomethionine Ameliorates Neuropathology in the Olfactory Bulb of a Triple Transgenic Mouse Model of Alzheimer's Disease.International journal of molecular sciences · 2016Article
- The Role of Cdk5 in Alzheimer's Disease.Molecular neurobiology · 2016Review
- Neuroprotective effects of Cerebrolysin in triple repeat Tau transgenic model of Pick's disease and fronto-temporal tauopathies.BMC neuroscience · 2015Article
- Cyclin-Dependent kinase 5 targeting prevents β-Amyloid aggregation involving glycogen synthase kinase 3β and phosphatases.Journal of neuroscience research · 2015Article
- Insights into the clinical value of cyclin-dependent kinase 5 in glioma: a retrospective study.World journal of surgical oncology · 2015Article
- p35 and Rac1 underlie the neuroprotection and cognitive improvement induced by CDK5 silencing.Journal of neurochemistry · 2015Article
- Therapeutic Actions of the Thiazolidinediones in Alzheimer's Disease.PPAR research · 2015Review
- Alteration of Golgi Structure by Stress: A Link to Neurodegeneration?Frontiers in neuroscience · 2015Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is the most common cause of dementia worldwide. One of the main pathological changes that occurs in AD is the intracellular accumulation of hyperphosphorylated Tau protein in neurons. Cyclin-dependent kinase 5 (CDK5) is one of the major kinases involved in Tau phosphorylation, directly phosphorylating various residues and simultaneously regulating various substrates such as kinases and phosphatases that influence Tau phosphorylation in a synergistic and antagonistic way. It remains unknown how the interaction between CDK5 and its substrates promotes Tau phosphorylation, and systemic approaches are needed that allow an analysis of all the proteins involved. In this review, the role of the CDK5 signaling pathway in Tau hyperphosphorylation is described, an in silico model of the CDK5 signaling pathway is presented. The relationship among these theoretical and computational models shows that the regulation of Tau phosphorylation by PP2A and glycogen synthase kinase 3β (GSK3β) is essential under basal conditions and also describes the leading role of CDK5 under excitotoxic conditions, where silencing of CDK5 can generate changes in these enzymes to reverse a pathological condition that simulates 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.