ArticleMolecular brain2013
Chronic overload of SEPT4, a parkin substrate that aggregates in Parkinson's disease, causes behavioral alterations but not neurodegeneration in mice.
Article in Molecular brain, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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20 citing papers in PubMed, 36 citations in OpenAlex.
- DYRK1A and Parkinson's disease, facts and hypotheses.Neurobiology of disease · 2026Review
- Investigating the Neuroprotective, Hepatoprotective, and Antimicrobial Effects of Mushroom Extracts.International journal of molecular sciences · 2025Article
- Comprehensive behavioral phenotyping of male Septin 3-deficient mice reveals task-specific abnormalities.Molecular brain · 2025Article
- Optogenetic elevation of postsynaptic cGMP in the hippocampal dentate gyrus enhances LTP and modifies mouse behaviors.Frontiers in molecular neuroscience · 2024Article
- miR-124-3p regulates the proliferation and differentiation of retinal progenitor cells through SEPT10.Cell and tissue research · 2023Article
- How Well Do Rodent Models of Parkinson's Disease Recapitulate Early Non-Motor Phenotypes? A Systematic Review.Biomedicines · 2022Review
- Article
- Dopaminergic Axons: Key Recitalists in Parkinson's Disease.Neurochemical research · 2022Review
- Septins, a cytoskeletal protein family, with emerging role in striated muscle.Journal of muscle research and cell motility · 2021Review
- Mice with mutations in Trpm1, a gene in the locus of 15q13.3 microdeletion syndrome, display pronounced hyperactivity and decreased anxiety-like behavior.Molecular brain · 2021Article
- A blueprint of septin expression in human tissues.Functional & integrative genomics · 2019Article
- Proteomic analysis of the effect of the polyphenol pentagalloyl glucose on proteins involved in neurodegenerative diseases in activated BV‑2 microglial cells.Molecular medicine reports · 2019Article
- miR-185 and SEPT5 Genes May Contribute to Parkinson's Disease Pathophysiology.Oxidative medicine and cellular longevity · 2019Article
- Twenty years since the discovery of the parkin gene.Journal of neural transmission (Vienna, Austria : 1996) · 2017Review
- Linking F-box protein 7 and parkin to neuronal degeneration in Parkinson's disease (PD).Molecular brain · 2016Review
- Age-related changes in behavior in C57BL/6J mice from young adulthood to middle age.Molecular brain · 2016Article
- A CDC42EP4/septin-based perisynaptic glial scaffold facilitates glutamate clearance.Nature communications · 2015Article
- Synaptic dysfunction and septin protein family members in neurodegenerative diseases.Molecular neurodegeneration · 2015Review
- Septin functions in organ system physiology and pathology.Biological chemistry · 2014Review
- [Functional Characterization of Septin Complexes].Molekuliarnaia biologiiaReview
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIn autosomal recessive early-onset Parkinsonism (PARK2), the pathogenetic process from the loss of function of a ubiquitin ligase parkin to the death of dopamine neurons remains unclear. A dominant hypothesis attributes the neurotoxicity to accumulated substrates that are exempt from parkin-mediated degradation. Parkin substrates include two septins; SEPT4/CDCrel-2 which coaggregates with α-synuclein as Lewy bodies in Parkinson's disease, and its closest homolog SEPT5/CDCrel-1/PNUTL1 whose overload with viral vector can rapidly eliminate dopamine neurons in rats. However, chronic effects of pan-neural overload of septins have never been examined in mammals. To address this, we established a line of transgenic mice that express the largest gene product SEPT4(54kDa) via the prion promoter in the entire brain.
resultsHistological examination and biochemical quantification of SEPT4-associated proteins including α-synuclein and the dopamine transporter in the nigrostriatal dopamine neurons found no significant difference between Sept4(Tg/+) and wild-type littermates. Thus, the hypothetical pathogenicity by the chronic overload of SEPT4 alone, if any, is insufficient to trigger neurodegenerative process in the mouse brain. Intriguingly, however, a systematic battery of behavioral tests revealed unexpected abnormalities in Sept4(Tg/+) mice that include consistent attenuation of voluntary activities in distinct behavioral paradigms and altered social behaviors.
conclusionsTogether, these data indicate that septin dysregulations commonly found in postmortem human brains with Parkinson's disease, schizophrenia and bipolar disorders may be responsible for a subset of behavioral abnormalities in the patients.
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