Range of brain diseases could be treated by single drug
By James Gallagher Health and science reporter, BBC News
The author of this article sites a new study, recently published in Nature (abstract link below), which details a possible new therapy for neurodegenerative diseases. If successful this drug could target numerous diseases including Parkinson’s, Alzheimer’s, Huntington’s, and prion diseases, such as the human form of mad cow disease. This study utilized a mouse model of prion disease. It is thought that the contributing factors to these diseases are accumulations of miss folded proteins. They showed that as misfolded protein levels rise in the brain, cells respond by trying to shut down the production of all new proteins through phosphorylation of the α-subunit of eukaryotic translation initiation factor, eIF2. Increased eIF2α-P levels are seen in neurodegenerative diseased patients. It is theorized that cell death might result because this arm of protein synthesis is shut down leaving cells unable to rebuild and replenish themselves. There data showed that increasing eIF2α-P levels, exacerbating neurotoxicity and significantly reducing survival in prion-diseased mice. While reducing eIF2α-P levels decreased neuronal death and increased survivability of the mice. Their results suggest that manipulation of common pathways such as translational control, rather than disease-specific approaches, may lead to new therapies preventing synaptic failure and neuronal loss across the spectrum of these disorders.
Certainly interesting work... I would like to see more data on the longevity of these studies. I wonder if other side effects would result due excessive protein buildup. In numerous papers we have read they mention the inflammatory response due to excessive protein deposits. Would this response be worsened, resulting in disease progression, if protein synthesis is not curbed? I wonder if a combination of therapies could be utilized to lessen side effects while improving disease prognosis?
Certainly this treatment sounds viable and like a fix, but as you said if you prevented this protein and the subunit elF2-P folding what implications might occur because of it?
ReplyDeleteAlso since since this article is geared towards Alzheimer's, Parkinson's, and neurodegenerative diseases in general I wonder if research that is discovered here can be put to the test in other diseases such as muscular and/or bone degeneration. I know other diseases as well result because of poor protein structure, maybe if the researchers find a preventative measure to stop protein malformation it can be a huge discovery in the field of medicine.