The CRTC1 protein and the FGF1 gene are critical for memory.
Researchers recently identified a molecular pathway that provides additional knowledge about memory difficulties in the elderly. These findings may also assist scientists in creating drug therapies to prevent the onset of dementia in the future, according to a study published by Cell Reports.
"Memory decline brings much suffering to the affected individuals and their families and leads to staggering social and economic costs," said study co-author Gleb Shumyatsky, PhD. "This work may provide scientists with answers and therapeutic help in the future for those going through normal aging or suffering from dementia."
The investigators found that signaling pathways in the hippocampus play an important, previously unknown role in dementia and other neurodegenerative diseases. The hippocampus is the part of the brain that controls memory and learning. Specifically, the researchers examined how information is transmitted from the synapses to the nuclei in neurons in the hippocampus.
In the study, the researchers discovered that the CRTC1 protein is able to improve memory by controlling gene expression in mice models. This process allows a cell to respond to a changing environment, and acts as a control for when and how much of a certain protein are released, according to the study.
"There is a potential that this could help with memory in the human brain," Dr Shumyatsky said. "We found that the longer the CRTC1 stays in the mouse brain, the stronger the memory."
The researchers then used fear conditioning and object location learning to evaluate memory in these mice. They discovered mice that had received extended amounts of training expressed more CRTC1.
Mice with a higher CRTC1 expression were also observed to have a more robust and powerful transcription, and had a better long-term memory, according to the study.
The investigators also found that CRTC1 activated the FGF1 gene that regulates brain cell growth and survival, and is crucial for repair and regeneration of damaged brain tissue.
Activating this gene was seen to improve memory in mice.
While memory declines naturally in a majority of aging individuals, this decline is more significant in those with Alzheimer’s disease and other similar conditions. These neurodegenerative diseases are largely due to disintegration of the brain’s communication mechanisms that are needed for optimal cognitive function, according to the study.
These findings may lead to novel treatments for neurodegenerative diseases. While much research has been done to determine the causes, no consistent biological deficits have been discovered as a viable treatment option.
Understanding molecular pathways in the brain, and how they affect each other, shows the potential to lead to effective treatment options for patients with Alzheimer’s disease, according to the study.
"The memory process is very much the same in both human and mouse brains," Dr Shumyatsky concluded. "Our group has been unraveling molecular mechanisms that maintain and improve memory, and what our research tells us is that there are different answers to controlling and improving memory."