Bacteria and viruses, with a genetic code that can be shared among them, could help scientists map out the evolution of the human brain.
The work was published Thursday in the journal Nature.
Researchers at the University of Pennsylvania, Pennsylvania State University, and the University at Buffalo have developed a method for generating “chromosomes,” which are microscopic structures that are part of cells and that are often shared among bacteria and viruses.
It’s an evolutionary model that’s used in molecular genetics, the study says, but this is the first time researchers have used the same method for predicting the disease risk of individuals based on their chromosomes.
“We have identified the basic principles of what makes chromosomes important for the function of cells,” said James S. Smith, a professor of biomedical engineering and the lead author of the study.
“If we could figure out what these fundamental principles are, then we could design a new way of identifying and studying the genes that are involved in aging, and we could then target those genes in an effective way to intervene in those processes.”
“If you can find a gene that is very close to having an effect on how cells function, you can start to develop therapies that target it, so we could treat disease by targeting the DNA that is related to aging,” Smith added.
“In fact, you could even use this to target genes that have the greatest impact on the onset of Alzheimer’s.”
Smith and his colleagues developed a way to identify a particular gene that was associated with a gene called the GATA4 enzyme.
This enzyme is responsible for breaking down proteins, and it also makes a protein called ATP, which is a powerful molecule that allows cells to use energy.
In a mouse model, this protein is linked to an enzyme called MTHFR, which helps the body break down proteins.
The researchers then showed that this enzyme is highly expressed in the brains of mice with Alzheimer’s disease, which causes cognitive decline.
They also showed that mice with the mutation had higher levels of MTHF, and that mice without the mutation also had higher MTHFs.
The mice with a mutation also developed Alzheimer’s at a younger age than mice with no mutation.
The team also showed in mice that the MTHG1 mutation increased the frequency of abnormal proteins, suggesting that this mutation is associated with increased MTHfr expression.
“Our work suggests that the GAT4-driven process of DNA methylation that occurs in cells could be a mechanism for determining disease risk,” Smith said.
“What we found is that a mutation in the GATOR3 gene can have a big impact on MTHf expression.
MTHs can be associated with inflammation and inflammation is associated in some studies with Alzheimer-related diseases.”
In addition to improving the understanding of how chromosomes function, the research could also be used to understand the origins of human intelligence.
“Genetic studies have shown that certain mutations that are associated with higher rates of cognitive decline have a role in aging,” said Jules Biederman, an assistant professor of neurology and neuroscience at the Penn State School of Medicine.
“So the discovery of this GAT3 mutation is a major step toward understanding this.
It will help us understand what are the mutations that cause brain aging and how they impact brain function.
It could also help us develop treatments that target these mutations.”
The study, which was published in Nature, involved four mouse models of Alzheimer, and they all exhibited Alzheimer’s symptoms, according to Biedermans work.
Smith said that these results are not meant to suggest that all individuals with the GATE1 mutation will develop Alzheimer’s, but rather to suggest the potential of this mutation to help prevent or treat Alzheimer’s.
“These results are really exciting,” Smith told FoxNews.com.
“It shows that we have a way of predicting that the rate of disease will be higher in mice genetically related to Alzheimer’s than in mice from people genetically related.”
While the findings have not been published in a peer-reviewed journal, they are already being used by scientists.
“This study has a huge impact on our understanding of the mechanisms underlying Alzheimer’s,” Biederal said.
The researchers say they are also investigating a possible application for this work in humans, where the researchers have tested the mice with mutations that prevent MTHH from making the protein ATP.
This could lead to a therapy that targets the MHTFR enzyme and might be used as a therapeutic strategy to treat Alzheimer.
