Video Transcript
Now, when we go to traumatic brain injuries, it’s, it gets even more complicated because now we’re dealing with, uh, a significant cellular issue. And like we were talking about during, before we started recording, if you, to really visualize traumatic brain injuries and like the process of how this becomes encephalopathy and dementia, like think of a neuron, like it’s made of Legos.
You have the branches up here, the dendrites, the axon, and as soon as it receives damage, this neuron, which is made of tau proteins, that’s what these Legos are made of, it shatters all over the floor. Now you’ve got all these Legos all over your floor. Now, Your brain’s normal response to that is to have your glial cells, which are the immune system of the brain.
They have a couple of different roles. Normally in a healthy brain, they just sit and they’re sitting there as a sentinel cell. When they see something like that happen, or they observe a foreign body. They go into what I call kill mode. It’s also called M1 activation. So they get activated, they see the contaminant or the body that they need to get rid of.
They shoot reactive oxygen species at it. So that could be like hydrogen peroxide is an example of a reactive oxygen species. Okay. There’s more than just that for the sake of this. We’ll keep it simple anyway. So they shoot reactive oxygen species at the foreign contaminant, and then they assume what’s called a phagocytic role, and they absorb it.
Now, that takes a lot of energy. Sure. So, like, you’re charging the gun, you’re firing it, you’re absorbing. If the cell doesn’t have, like, enough energy to do that, it doesn’t absorb. Basically just gets stuck in kill mode. Sure. So it racks the mod deuce and just starts pumping reactive oxygen species downrange now That’s happening at scale.
We’re talking about millions of cells doing this at a time So now you’ve got all these legos floating around in free space These reactive oxygen species are being spit into that space and they’re coding these legos. It’s called tau hyperphosphorylation And once that happens, these Legos are now coated in this sticky goo that is toxic, and they stick together.
Okay. They’re floating around and just gathering up in these large balls. Sure. They’re called neurofibrillary tangles, and they get bigger and bigger and bigger. It’s pretty, pretty much like, just for the audience to recognize when you have too much mucus that builds up. Yeah. Right? It becomes a cascading effect.
Mm hmm. In a negative fashion. Yep, and eventually, these tangles get so big that they interfere with the signaling. So your brain doesn’t have a lymph system, so there’s no way to, like, get rid of these foreign bodies, right? There’s several things you can do. I mean, your brain, technically, when you’re sleeping, and this is why sleep is so important, your cerebrospinal fluid, you know, exchanges.
Flushing. Yeah, it flushes out. One of the primary issues with TBI is that sleep is typically affected pretty negatively, so then you get stuck in a scenario where Now you’ve got all of these legos together. Recycling and taking out the trash happens when you’re sleeping. And if your sleep is off, you’re not going through that rhythm.
You’re not going through the cleaning cycle and boom, it’s gonna be gummed up. Sure. That whole process, it’s not quick. You can be in that state of microglial priming. For years, it literally lasts until it kills you. So that’s why you see someone who like they have a TBI, they’ll get a little bit better, then they plateau and then all of a sudden it’s like boom.
That’s when those neurofibrillary tangles start interfering with those neurons.