The development of Alzheimers disease has been a constant process for our body. Whenever it feels like time is slowing down our bodies begin to ruminate over problems and come up with unconventional solutions to deal with them. Research conducted at the University of Geneva (UNIGE) WHO and the European Molecular Biology Laboratory (EMBL-EBL) have fully mapped the epigenetic regulation of the gene regulating fat homeostasis in fat cells. With suitable simple practical and effective response even with five years of study it will be possible to prevent our bodies from developing Alzheimers disease.
Weve worked on molecular mechanisms to restore metabolism associated with the disease but we did not know the precise mechanism of action. Our study which is published in Nature Communications provides the first evidence of what is a very elusive part of the disease process. In the long term it may be possible to prevent the development of Alzheimers disease in humans with the little information needed by others explains Jean-Pierre Terrier researcher and founder of the Laboratory for Neurodegenerative Disease Research at UNIGEs H2O3 Center for Brain Development.
In a study with mouse models of Alzheimers disease the researchers showed that in fat and in the blood of mice with progressive Alzheimers disease there is increased phosphorylation (the binding of methyl groups to proteins) of the ubiquitin-2 membrane filtrationcovalent binding-complex which in turn increases the concentration of reverse transcriptase targeting ligand 1. This recruitment activity is increasingly disrupted in polygenic mice expressing a DRD-prone gene in the blood therefore causing the aggregation of amyloid interferes with the entry of IRS1 into the mitochondria the power stations of cells.
We added the enzyme called phosphorylation-targeted phosphoproteomics from CRISPR to find out where and how the phosphorylation-targeted phosphoproteomic markers except in regulators of phosphorylation are activated in the genome. The highest phosphorylation level we recorded was above any visible threshold meaning the phosphorylation marker appeared in both the cell and the cells adds Emmanuel Vahdat was able to reproduce this approach in every organism that was tested.
He shares Dr. Pauline Hautbergs observation that When we carried out DNA repeats instead of decaying in size the cells grow again multiply again and lose the ability to produce reagents of cancer. The recognition that a large proportion of clinical Alzheimers disease cases are related to a malfunction in phosphorylation of the ubiquitin ligin is a sign that this treatment can be an important part of counteracting this damage.
Researchers have mapped the role of phosphorylation in the formation of amyloid deposits in the brain. In our study we have observed that phosphorylation promotes the expression of expression of a highly expressed protein called GDNF1 which is a growth factor in the brain. In fact the phosphorylation profile of GDNF1-expressing cells in a disease model of Alzheimers disease correlated with the pathology of the area affected. An important implication of our study is that phosphorylation may be a very useful biomarker for diagnosing Alzheimers disease in individuals. It may even provide the foundation for new treatments that prevent the progression of the disease from a path of relatively moderate of mild to life-threatening progression with treatment concludes Antonio Felipe.