ReviewActa neuropathologica2015
Physiological and pathophysiological functions of cell cycle proteins in post-mitotic neurons: implications for Alzheimer's disease.
Review in Acta neuropathologica, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 2 of them syntheses that pooled it.
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
35 citing papers in PubMed, 2 syntheses or guidelines pooled it, 64 citations in OpenAlex.
- Prediction of differentially expressed microRNAs in blood as potential biomarkers for Alzheimer's disease by meta-analysis and adaptive boosting ensemble learning.Alzheimer's research & therapy · 2021Pooled it
- Systematic Review of miRNA as Biomarkers in Alzheimer's Disease.Molecular neurobiology · 2019Pooled it
- Nuclear Translocation of IGF1R Induces Cell Cycle Re-entry via Cyclin D1 Regulation in an Aβ-Driven Alzheimer's Disease Model.Molecular neurobiology · 2026Article
- Review
- Loss of AT8 Nuclear Tau as a Marker of Neuronal Ageing and Alzheimer's Disease Progression.Biomedicines · 2025Article
- Article
- Uncovering Cell Cycle Dysregulations and Associated Mechanisms in Cancer and Neurodegenerative Disorders: A Glimpse of Hope for Repurposed Drugs.Molecular neurobiology · 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
- DNA Damage Response-Associated Cell Cycle Re-Entry and Neuronal Senescence in Brain Aging and Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2023Review
- FISHing for Chromosome Instability and Aneuploidy in the Alzheimer's Disease Brain.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Neurons burdened by DNA double-strand breaks incite microglia activation through antiviral-like signaling in neurodegeneration.Science advances · 2022Article
- Article
- Oncogenic Pathways in Neurodegenerative Diseases.International journal of molecular sciences · 2022Review
- p27, The Cell Cycle and Alzheimer´s Disease.International journal of molecular sciences · 2022Review
- Postoperative Cognitive Dysfunction and Alzheimer's Disease: A Transcriptome-Based Comparison of Animal Models.Frontiers in aging neuroscience · 2022Article
- Polymerases and DNA Repair in Neurons: Implications in Neuronal Survival and Neurodegenerative Diseases.Frontiers in cellular neuroscience · 2022Review
- Unraveling the links between neurodegeneration and Epstein-Barr virus-mediated cell cycle dysregulation.Current research in neurobiology · 2022Review
- METTL3-dependent RNA mMolecular neurodegeneration · 2021Article
- Review
- Rapid initiation of cell cycle reentry processes protects neurons from amyloid-β toxicity.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is the most prevalent neurodegenerative disorder for which no effective treatment is available. Increased insight into the disease mechanism in early stages of pathology is required for the development of a successful therapy. Over the years, numerous studies have shown that cell cycle proteins are expressed in neurons of AD patients. Traditionally, neurons are considered to be post-mitotic, which means that they permanently retract from the cell cycle. The expression of cell cycle proteins in adult neurons of AD patients has therefore been suggested to promote or even instigate pathomechanisms underlying AD. Interestingly, expression of cell cycle proteins is detected in post-mitotic neurons of healthy controls as well, albeit to a lesser extent than in AD patients. This indicates that cell cycle proteins may serve important physiological functions in differentiated neurons. Here, we provide an overview of studies that support a role of cell cycle proteins in DNA repair and neuroplasticity in post-mitotic neurons. Aberrant control of these processes could, in turn, contribute to cell cycle-mediated neurodegeneration. The balance between regenerative and degenerative effects of cell cycle proteins in post-mitotic neurons might change throughout the different stages of AD. In the early stages of AD pathology, cell cycle protein expression may primarily occur to aid in the repair of sublethal double-strand breaks in DNA. With the accumulation of pathology, cell cycle-mediated neuroplasticity and neurodegeneration may become more predominant. Understanding the physiological and pathophysiological role of cell cycle proteins in AD could give us more insight into the neurodegenerative process in AD.
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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 OpenQuestion graph.