For centuries, it has been accepted that wisdom comes as we age. This has been solidly supported by a variety of acetic philosophies and cultures over the eons. Science has been working for countless years to solve the problems that come about because of human aging. Because science is always seeking to expand our knowledge of the unknown, we are slowly beginning to make progress in understanding aging, and maybe a new discovery will open new doors to solving the human events connected to aging. Nature Shows just published an online study dealing with SIRT1 and how it is involved in learning and memory.
SIRT1 is a protein and becomes involved in a number of actions of the human system, but in this study it is important to understand how the protein adjusts gene activity and has been shown to control metabolism. It has also been found that many of the biological processes causing aging are influenced by SIRT1. Li-Hui Tsai, a neuroscientist at Howard Hughes Medical Institute, and MIT designed a new study to investigate SIRT1’s role in learning and memory. This is an animal study using mice. Dr. Tsai and her team have been given reason to believe SIRT1 has a role in the brain based on their examining earlier studies. Resveratrol is an activator of SIRT1, which could help neurons survive a mouse’s version of Alzheimer’s disease. It has been shown that resveratrol can improve a mouse’s capacity to learn and remember. Resveratrol is unique because it can act on all 7 sirtuins in mammals and influence the other biological processes. The scientist’s discovered the role of SIRT1 in this process.
Study design called for the study to use mice genetically engineered to lack SIRT1 in their brains. The mice were then exposed to a number of tests. In the tests they displayed Synapse xt problems of remembering the location of a submerged platform in a water maze, and demonstrated a number of problems in learning and memory tests. The testing clearly established the fact the mice were learning impaired. To gain a better understanding of exactly what the problems were, Tsai and her team had to examine the brains of the mice lacking SIRT1. When they examined a representative sample of mice brains, they found the brains lacked the healthy number of synapses or connections between neurons and as the number of synapses is reduced, it becomes more difficult for the mice to create long-term memories. This was the key clue to what molecules might be implicated to cause the loss of long-term memory. The team’s research also caused them to find the mice short on SIRT1 did not have an adequate level of a protein called CREB in their brains. CREB is important because it helps manage proteins necessary to regulate the needed strength of synapse between neurons.
As the team investigated in more detail, it was discovered SIRT1 modulates the CREB with a small piece of RNA named microRNA-134. It is also known as miR-134. Normally, a healthy mouse has an adequate amount of SIRT1 and a protein called YY. These two team up to control production of miR-134, but if the mouse does not have SIRT1, the brain requires more miR134 to be made. MicroRNA receives instructions for producing CREB and stops the production of the CREB protein.
Tsai’s research has reinforced SIRT1 as a master regulatory molecule which directs a number of aspects of the metabolism and cell function. Another scientist has been conducting another study in the same area as Tsai. Valter Longo is at the University of Southern California in Los Angeles. Valter does not believe it is a good idea to increase the brain’s level of SIRT1. Valter’s mice did not improve their memory when tested after having their SIRT1 boosted. Valter’s previous research data indicates that it would not be wise to increase the SIRT1 as it is not good for neurons.