Alzheimer’s disease is one of the most prevalent neurodegenerative diseases in America. It is commonly known as Type III diabetes due to the prevalence of insulin resistance in most Alzheimer’s patients. Treating Alzheimer’s disease has been a difficult task for researchers and physicians so far however there does appear to be hope for the future. Researchers believe to be pin-pointing the causal pathway leading to the onset of Alzheimer’s disease via the PI3-kinase/Akt pathway.
Many teenagers in America have witnessed the effects of Alzheimer’s disease whilst cuddling on a couch in their significant other’s basement watching the famed Nicholas Sparks movie “The Notebook”, and crying along as the emotional roller coaster brought them from sadness to happiness and back to immense sadness. (FULL DISCLOSURE: I never cried watching the movie though my girlfriend (who forced me to watch it in the first place did. However I will admit I did enjoy it more than I could ever admit to her.) The neurodegenerative disease opened a divide between two lovers as one began to forget all about their time together. Sadly, not everyone in world has the luxury of experiencing the disease through the TV screen, and is able to just turn it off when the credits start to roll. Others experience it first hand or watch as their loved ones slowly fade away into a shell of their own existence. What makes the disease so troublesome is that it tends to have a late onset in life and thus there isn’t much of an initiative to put an end to it or prevent it earlier in life.
Alzheimer’s disease occurs from neurodegeneration caused by the build-up of Amyloid Beta (Aβ) plaques in synapses. This is believed to be caused by an overactive IGF-1R/IR receptor leads to an over activated PI3-kinase/Akt pathway. This pathway leads to the over-activation of mTOR (a protein kinase that activates other important “effector proteins” via phosphorylation) leading to over phosphorylation of other pathways in the cell, causing cellular distress. Some current medications in clinical trials are aimed at inhibiting mTOR in an effort to slow down the accumulation of Aβ in intercellular spaces. Other drugs in trials are inhibiting one of the “effector proteins” (known as: S6K) that mTOR activates. By inhibiting S6K, less over-phosphorylation will occur within the cell leading to less accumulation of Aβ. Our neurons depend on well-balanced cellular concentrations of various proteins and signal molecules in order to function correctly. When these concentrations fall out of their ideal range of operation, pathways can become over-active thus leading to neuronal death.
Currently there is a growing initiative to prevent the onset of Alzheimer’s the same way we prevent type II diabetes, a well-balanced diet. Insulin resistance is common in patients with Alzheimer’s causing changes in cellular concentrations of insulin (commonly involved in neuronal pathways like the PI3-kinase/Akt pathway being studied here). Diet must be well-monitored and well-balanced throughout life especially in the later stages of our lives. Reducing our caloric intake later in life using a well-balanced diet can reduce our chances of developing Alzheimer’s.
If this knowledge can lead to more of an understanding of the connection between our diets and our health, maybe we can all save future generations from the wrath of sad love novels driven by neurodegenerative diseases by Nicholas Sparks.
Until Next Time,
Sebastian
Alzheimer's: Beyond Nicholas Sparks
