Katharina Buczek
In the past, his team specifically analyzed the chemical reaction– a process known as protein S-nitrosylation– that ultimately forms the modified form of complement C3.
The process essentially begins when a nitric oxide (NO) molecule tightly binds to a sulfur atom (S) on one distinct amino acid building block to create a modified “SNO-protein” form.
Now, within cells, it is common for small clusters of atoms– like NO– to undergo protein modifications. These changes usually work to activate or deactivate the function of a target protein.
However, Lipton suspected that these modifications– coined as “SNO-storms”– might be a critical contributor to the development of Alzheimer’s as well as other neurodegenerative disorders.
So, for his most recent study, Lipton and his team utilized novel S-nitrosylation detection techniques to quantify the number of modified proteins in the brains of forty deceased individuals.
Half of the individuals had died of AD, and the other half did not. Each group was also segmented equally between males and females.
The scientists found that over 1,400 different proteins had been S-nitrosylated within these brains.
Most notably, though, the presence of S-nitrosylated C3 (SNO-C3) was found to be over 600% higher among females who died of AD as opposed to males who died of AD.
It has been known for over three decades that the brains of Alzheimer’s patients contain higher levels of complement proteins, as well as other inflammation markers.
However, research in recent years has shown that complement proteins can actually trigger immune cells in the brain– known as microglia– to destroy synapses.
In other words, the neural network connection points that neurons use to communicate via signals.
