Dysfunctional Golgi Apparatus Implicated in Some Forms of Neurodegeneration

Researchers have shown that dysfunction in Golgi apparatus organelles in brain cells is important in some forms of neurodegenerative disease, and identified a controlling protein that might be used in order to partially reverse this dysfunction. The Golgi apparatus is involved in the later stages of production and deployment of protein machinery in the cell; it packages up proteins for dispatch to their destination inside the cell, or for secretion outside the cell. Some past research has suggested relevance for Golgi apparatus failure in Alzheimer's disease, and there are indications that Golgi function might be one of the factors determining differences in species longevity.

Researchers have identified the early neuropathic mechanism of polyglutamine brain disease, one of the representative degenerative brain diseases, and suggested a way to restore it. It is expected to accelerate the development of the early neuropathy treatment for a variety of degenerative brain diseases. The research teams have verified for the first time in the world 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 these 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. In addition, by identifying the transcription factors involved in the early neuropathy caused by toxic proteins such as CrebA and high-level factor CREB-binding protein, the researchers have suggested that they could be new subjects to develop therapeutic agents for degenerative brain diseases.

Link: http://en.dgist.ac.kr/site/dgist_eng/menu/508.do?siteId=dgist_eng&snapshotId=3&pageId=429&cmd=read&contentNo=35010


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