I have previously written about research that delves into episodic memory loss, which is the type of memory loss typically associated with Alzheimer’s disease.
While most studies of potential Alzheimer’s drugs examine how these compounds affect spatial memory, it is episodic memory — the ability to remember specific events — that is most affected by the disease. Episodic memory impairment is also associated with aging in general.
The above research was conducted on rats who were trained to memorize up to twelve different odors in a specific order. The results of the experiment pointed to strong evidence that the animals were employing episodic memory replay. It is encouraging for researchers to have these animal models of episodic memory that appear to be comparable to the way human episodic memory works.
Another study published in April 2018 in the Journal of Neuroscience has taken things one step further. Researchers at Drexel University have actually reversed symptoms of Alzheimer’s disease in an animal model by focusing on the levels of two enzymes that are believed to have an epigenetic influence. Briefly, epigenetics is the study of changes in gene expression that do not involve alterations to DNA, but rather are attributed to our experiences and possibly even our thoughts and feelings. You can read more about epigenetics here.
In the April 2018 study researchers focused on the HDAC2 enzyme, which plays a role in the expression of genes that relate to learning and memory. It is often thought that cognitive issues related to the early stages of Alzheimer’s disease are connected to an increase in the levels of the HDAC2 enzyme. When the levels of this enzyme increase, they throw levels of another enzyme, Tip60HAT, off balance, and the result is a disruption in proper gene regulation. The expression of certain genes then decreases and the brain’s ability to recall and/or process information is negatively affected.
In their experiment, researchers at Drexel University added Tip60HAT to the brains of flies that were models of Alzheimer’s disease. Results showed that the enzymatic balance was restored and the flies were then not only able to learn new things but also remember them — thus indicating the dysfunction had been corrected. In addition, the scientists also looked at the effects of the additional Tip60 HAT on genes that aid in brain function and are down-regulated by elevated HDAC2 levels. Not surprisingly, the supplemental Tip60 HAT elevated nine of eleven genes back to normal expression levels. These results certainly give us reason to believe that gene therapy might be a viable way to treat Alzheimer’s disease.
Associate professor Felice Elefant, Ph.D., who worked on the study, said:
When people age, they have a loss of memory but it’s not because there are mutations in their genes. It’s the way they’re packaged. They’re distorted. And we’re seeing non-invasive ways we might be able to prevent that early on.
Right now there is no cure for Alzheimer’s disease, but research such as this should give us all hope for better treatments down the road, and maybe someday, we’ll even be able to prevent the development of this devastating disease.