Alzheimer’s Disease (AD) is a disease that is infamous to many. The devastating effect it can have one an individual and those around them along with the high prevalence rate has lead to this disease being a hot topic for research.
In an article by O’ Neill, the PI3K and mTOR pathway was examined as likely culprits, if at the very lease accomplices in this nasty brain disease. The article explains that the PI3K pathway is activated by insulin which then leads to an increase in mTOR, which is a receptor or rapamycin. This increase then leads to a protein called Tau becoming phosphorylated.
Phosphorus in the body acts as a switch either turning on or off a protein. In the case of Tau, phosphorylation acts an activator of this protein, and with these new modifications this protein becomes a dangerous one. Phosphorylated Tau leads to neurofibulary tangles (NFT), which act as road blocks in the brain. With synapses having a harder time connecting with one another, neurons start to weaken and eventually die.
As bleak as this pathway may seem, the uncovering of PI3K in the role of AD does have promising implications. Studies have been shown that exercise can help lower the amount of phosphorylated Tau, which means less NFTs which cause the cognitive decline in individuals.
Currently in the US, there is a study that is in the recruiting stages that’s goal is to uncover which kinds of exercise can help support memory. Ultimately, they are looking for exercises that can be given to individuals to help treat and prevent AD . Although the role an over-activated PI3K/ mTOR pathway can have detrimental effects, the discovery of this pathway in AD can help us understand what causes this form of dementia and hopefully what can treat it.
For more reading on the PI3K pathway check out:
For more reading on the current US trial with exercise and AD check out: