Researchers have identified the early neuropathic mechanism of dendritic-specific Golgi on neurodegenerative brain diseases in neuronal cells for the first time in the world.
The research teams have verified for the first time that dendritic-specific Golgi, one of the cellular organelles in neurons, plays a key role in early neuropathy of degenerative brain disease.
In a model of degenerative brain diseases such as Huntington's chorea and spinal cord cerebellar degeneration that are caused by polyglutamine toxic protein, the research teams identified that deformation or abnormality of dendritic-specific Golgi, which plays a key role in supplying the cell membrane of brain cells, is the major cause of degenerative brain disease as it leads morphological transformation of neuronal cells.
In this morphologically modified brain cells, the study has demonstrated that the early neuropathy of diseased brain cells can be restored by inducing overexpression of the CrebA gene, the newly discovered key factor in pathology. CrebA expression is regulated by CREB-binding protein (CBP), which is sequestered by polyQ proteins. Furthermore, co-overexpression of CrebA and Rac1 synergistically restored the polyglutamine-induced dendrite pathology.
Senior author said "The key of this study is that we have verified that dendrite-specific Golgi of brain cells plays a core role in the early neuropathy of degenerative brain disease," and added "By restoring the early stages of the disease, we expect to accelerate the development of therapeutic drugs that can effectively treat degenerative brain diseases."
This study has been published in the journal Cell Reports.
http://www.cell.com/cell-reports/abstract/S2211-1247(17)30890-2
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