Katharina Buczek
Instead of firing when stimulated, hyperexcited neurons will continuously fire. This can cause neural network dysfunction, cognitive decline, and seizures.
So, after identifying this link to AD, Professor Ittner and his researchers then set their sights on other diseases in which hyperexcitation is at play– such as epilepsy.
Built-up hyperphosphorylated tau proteins in brain microtubules have been associated with numerous neurological diseases, including several kinds of dementia.
When the phosphorylation process functions properly, it acts as a “fine-tuner,” which allows for communication between proteins.
So, when phosphoryl is in the right quantity and at the right location, it is critical for the maintenance of signaling pathways in the brain.
Too much phosphoryl, though, can have damning and toxic effects.
After a protein molecule becomes hyperphosphorylated, too much phosphoryl will stick to the protein’s surface– ultimately changing its shape and impacting the protein’s ability to bind and communicate.
Typically, phosphoryl will act as a sort of lubricant, allowing for molecules to slip apart. According to Professor Ittner, this process is similar to when hair is washed down a shower drain.
The drain can handle a few hairs at a time. But, when there is a significant build-up, they will clump together and block the pipe.
In the human brain, though, this “pipe” is actually the human neuron. And once the pipe to a neuron is blocked off, it will die– and there is currently no treatment out there to regenerate neurons.
The team’s new study, though, found that when the phosphorylation of tau protein by kinase p38y takes place at a specific location within the genome, known as Threonine 205, excitotoxicity can actually be prevented– in other words, what causes seizures.
