Last month, the University was once again the leader in groundbreaking medical research with a new study from the School of Public Health that discovered a change in Alzheimer’s patient’s brain structure.
In a collaborative study that performed a postmortem analysis on subjects with and without Alzheimer’s, researchers from nine different University departments found a change in the epigenome — responsible for turning genes on and off — of Alzheimer’s patients.
Dana Dolinoy, assistant professor in the Public Health School and the study’s co-author, specializes in epigenetics and said that if the genome is a computer, the epigenome would be the software that tells it what to do.
According to Dolinoy, this discovery is important because it allows for research of new ways to treat or prevent Alzheimer’s disease.
“If a disease is caused by an epigenetic effect we may be able to use dietary approaches or pharmacological treatments to counteract the negative epigenetic effect,” Dolinoy said.
She added that, apart from treatment methods, this research is important in helping identify who will have the disease earlier than could be done before.
According to Howard Hu, chair of the department of environmental sciences in the Public Health School and principal investigator on the study, changes in the epigenome can be caused by environmental factors early in life like exposure to toxic chemicals.
Though this study did not examine specific causes for the change in epigenome, Hu believes that exposure to lead could be an important factor in triggering the change in the epigenome, but added that this hypothesis requires further research.
“Basically, we are now setting the stage for doing research on early-life risk factors for changing the epigenome in a benchmark area of the brain that we have shown is associated with Alzheimer’s later in life,” Hu said.
Because these findings are groundbreaking, Hu added that the study will need to be replicated in order to ensure its validity, but he believes it made great strides toward understanding Alzheimer’s disease.
Apart from the epigenomic differences found, researchers also discovered increased amounts of the protein TMEM59 in subjects with Alzheimer’s.
The found changes in the epigenome lead to fewer methylated genes as well as an increase in the TMEM59 protein, according to Dolinoy. She explained that methylation is a mechanism that controls the strength of a gene like a dimmer switch on a light, in this case decreasing the strength of TMEM59 in Alzheimer’s patients.
Dolinoy believes the discovery of the lower methylation and increased TMEM59 protein is important for validating the results they found.
“It’s along the mechanism pathway,” Dolinoy said. “It’s a validation of the central dogma: We went from DNA to RNA to protein. You want to be able to say that the epigenome also had an effect at the protein level.”