ArticleBrain : a journal of neurology2011
Schizophrenia is associated with dysregulation of a Cdk5 activator that regulates synaptic protein expression and cognition.
Article in Brain : a journal of neurology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 1 of them a synthesis that pooled it.
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Who cites it
60 citing papers in PubMed, 1 synthesis or guideline pooled it, 107 citations in OpenAlex.
- The role of septin 7 in physiology and pathological disease: A systematic review of current status.Journal of cellular and molecular medicine · 2018Pooled it
- Seeing elephants and drinking water from a porcelain vase - A case of septin-7 antibody-associated encephalitis presenting as a severe disorganized psychosis.Translational psychiatry · 2026Article
- Memory-Associated Immediate Early Genes: Roles in Synaptic Function, Memory Processes, and Neurological Diseases.Molecular neurobiology · 2025Review
- Circulating Cathepsin D Exacerbates Injury-Induced Brain Damage by Promoting Neutrophil Infiltration Into the Brain.Journal of the American Heart Association · 2025Article
- Bioinformatics Analysis of Persistent Dysregulated Expression of Genes Involved in HCV-Induced Neurological Disorders and Liver Injuries After DAA Treatment Through Weighted Gene Co-Expression Network Analysis.Health science reports · 2025Article
- Article
- Contributions of major tau kinase activation and phospho-tau accumulation to cortical and hippocampal tangle formation and cognition in older adults.Neurobiology of disease · 2025Article
- Npbwr1 signaling mediates fast antidepressant action.Molecular psychiatry · 2025Article
- Transthyretin Orchestrates Vitamin B12-Induced Stress Resilience.Biological psychiatry · 2025Article
- WTAP-mediated mRedox report : communications in free radical research · 2024Article
- Mitochondrial dysfunction in psychiatric disorders.Schizophrenia research · 2024Review
- Neurogenic Effects of Inorganic Arsenic and Cdk5 Knockdown in Zebrafish Embryos: A Perspective on Modeling Autism.International journal of molecular sciences · 2024Review
- Epigenetic regulation of beta-endorphin synthesis in hypothalamic arcuate nucleus neurons modulates neuropathic pain in a rodent pain model.Nature communications · 2023Article
- Synaptic scaling of corticostriatal circuits underlies hyperactivity in GABA Transporter-1 deficient mice.iScience · 2023Article
- A Postsynaptic Density Immediate Early Gene-Based Connectome Analysis of Acute NMDAR Blockade and Reversal Effect of Antipsychotic Administration.International journal of molecular sciences · 2023Article
- Valproic Acid-Induced Anxiety and Depression Behaviors are Ameliorated in p39 Cdk5 Activator-Deficient Mice.Neurochemical research · 2022Article
- Involvement of Cdk5 activating subunit p35 in synaptic plasticity in excitatory and inhibitory neurons.Molecular brain · 2022Article
- Altered resting-state functional connectivity in hiPSCs-derived neuronal networks from schizophrenia patients.Frontiers in cell and developmental biology · 2022Article
- Inhibition of Cdk5 in PV Neurons Reactivates Experience-Dependent Plasticity in Adult Visual Cortex.International journal of molecular sciences · 2021Article
- Structure-Based Design and Optimization of FPPQ, a Dual-Acting 5-HTJournal of medicinal chemistry · 2021Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Cyclin-dependent kinase 5 is activated by small subunits, of which p35 is the most abundant. The functions of cyclin-dependent kinase 5 signalling in cognition and cognitive disorders remains unclear. Here, we show that in schizophrenia, a disorder associated with impaired cognition, p35 expression is reduced in relevant brain regions. Additionally, the expression of septin 7 and OPA1, proteins downstream of truncated p35, is decreased in schizophrenia. Mimicking a reduction of p35 in heterozygous knockout mice is associated with cognitive endophenotypes. Furthermore, a reduction of p35 in mice results in protein changes similar to schizophrenia post-mortem brain. Hence, heterozygous p35 knockout mice model both cognitive endophenotypes and molecular changes reminiscent of schizophrenia. These changes correlate with reduced acetylation of the histone deacetylase 1 target site H3K18 in mice. This site has previously been shown to be affected by truncated p35. By restoring H3K18 acetylation with the clinically used specific histone deacetylase 1 inhibitor MS-275 both cognitive and molecular endophenotypes of schizophrenia can be rescued in p35 heterozygous knockout mice. In summary, we suggest that reduced p35 expression in schizophrenia has an impact on synaptic protein expression and cognition and that these deficits can be rescued, at least in part, by the inhibition of histone deacetylase 1.
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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.