ReviewNeural regeneration research2023
Cdk5 and aberrant cell cycle activation at the core of neurodegeneration.
Review in Neural regeneration research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
20 citing papers in PubMed, 35 citations in OpenAlex.
- Mitochondrial Fission and Fusion Disorders and Autophagy Abnormalities in Parkinson's Disease.Neurochemical research · 2026Review
- Metabolic reprogramming in diabetes and other endocrine and metabolic disorders: exploring the Warburg effect, ketones, and SGLT2 inhibitors.Reviews in endocrine & metabolic disorders · 2026Review
- A patent review of cyclin-dependent kinase 5 (CDK5) inhibitors (1999-2025).Frontiers in bioengineering and biotechnology · 2026Review
- Article
- Salidroside derivative SHPL-49 enhances synaptic remodeling in BCCAO rats via the CDK5/p35/p25 signaling pathway.Frontiers in pharmacology · 2026Article
- CDK5 Inhibits Synphilin-1 Ubiquitination and Basal Mitophagy: Implications for Parkinson's Disease.International journal of molecular sciences · 2025Article
- Hepatocytes as Model for Investigating Natural Senotherapeutic Compounds and Their Effects on Cell Cycle Dynamics and Genome Stability.International journal of molecular sciences · 2025Review
- Multidimensional Evaluation of the Streptozotocin-Induced Alzheimer's Model: Integrating Molecular, Histopathological, and Behavioral Correlates Over Time.Neurochemical research · 2025Article
- Unravelling the Proteinopathic Engagement of α-Synuclein, Tau, and Amyloid Beta in Parkinson's Disease: Mitochondrial Collapse as a Pivotal Driver of Neurodegeneration.Neurochemical research · 2025Review
- Melittin promotes the proliferation of Schwann cells in hyperglycemic environment by up‑regulating the Crabp2/Wnt/β‑catenin signaling pathway.Molecular medicine reports · 2025Article
- New molecular mechanisms to explain the neuroprotective effects of insulin-like growth factor II in a cellular model of Parkinson's disease.Journal of advanced research · 2025Article
- Potential Roles of Hypoxia-Inducible Factor-1 in Alzheimer's Disease: Beneficial or Detrimental?Antioxidants (Basel, Switzerland) · 2024Review
- Mechanisms of autophagy-lysosome dysfunction in neurodegenerative diseases.Nature reviews. Molecular cell biology · 2024Review
- Protein Kinase C-Delta Mediates Cell Cycle Reentry and Apoptosis Induced by Amyloid-Beta Peptide in Post-Mitotic Cortical Neurons.International journal of molecular sciences · 2024Article
- Neuronal double-stranded DNA accumulation induced by DNase II deficiency drives tau phosphorylation and neurodegeneration.Translational neurodegeneration · 2024Article
- The pathogenic mechanism of TAR DNA-binding protein 43 (TDP-43) in amyotrophic lateral sclerosis.Neural regeneration research · 2024Review
- Effects of PMToxicology research · 2024Article
- Dual-specificity protein phosphatase 6 (DUSP6) overexpression reduces amyloid load and improves memory deficits in male 5xFAD mice.Frontiers in aging neuroscience · 2024Article
- A Review on Tau Targeting Biomimetics Nano Formulations: Novel Approach for Targeting Alzheimer's Diseases.Central nervous system agents in medicinal chemistry · 2024Review
- The role of epigenetic modifications in sensory hair cell development, survival, and regulation.Frontiers in cellular neuroscience · 2023Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neurodegenerative diseases are caused by the progressive loss of specific neurons. The exact mechanisms of action of these diseases are unknown, and many studies have focused on pathways related to abnormal accumulation and processing of proteins, mitochondrial dysfunction, and oxidative stress leading to apoptotic death. However, a growing body of evidence indicates that aberrant cell cycle re-entry plays a major role in the pathogenesis of neurodegeneration. The activation of the cell cycle in mature neurons could be promoted by several signaling mechanisms, including c-Jun N-terminal kinases, p38 mitogen-activated protein kinases, and mitogen-activated protein kinase/extracellular signal-regulated kinase cascades; post-translational modifications such as Tau-phosphorylation; and DNA damage response. In all these events, implicated Cdk5, a proline-directed serine/threonine protein kinase, seems to be responsible for several cellular processes in neurons including axon growth, neurotransmission, synaptic plasticity, neuronal migration, and maintenance of neuronal survival. However, under pathological conditions, Cdk5 dysregulation may lead to cell cycle re-entry in post-mitotic neurons. Thus, Cdk5 hyperactivation, by its physiologic activator p25, hyper-phosphorylates downstream substrates related to neurodegenerative diseases. This review summarizes factors such as oxidative stress, DNA damage response, signaling pathway disturbance, and Ubiquitin proteasome malfunction contributing to cell cycle re-entry in post-mitotic neurons. It also describes how all these factors are linked to a greater or lesser extent with Cdk5. Thus, it offers a global vision of the function of cell cycle-related proteins in mature neurons with a focus on Cdk5 and how this protein contributes to the development of Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and Huntington's disease by cell cycle activation.
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Registered trials
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 Socratic graph.