. A lot of scientific jargon can be tedious, like the next paragraph. I read this stuff and hear real english. It's just real english filled with a lot of "when this stuff is replaced by that stuff, it makes the new stuff that that stuff and this stuff makes, resist breaking down." Believe it or not, bigger words are easier to follow.
. "Transmissible spongiform encephalopathies (TSEs), also known as prion diseases, are a group of progressive conditions that affect the brain and nervous system of many animals, including humans. According to the most widespread hypothesis they are transmitted by prions, though some other data suggest an involvement of a Spiroplasma infection. Mental and physical abilities deteriorate and myriad tiny holes appear in brain tissue. The disorders cause impairment of brain function, including memory changes, personality changes and problems with movement that worsen over time. Prion diseases of humans include classic Creutzfeldt–Jakob disease, new variant Creutzfeldt–Jakob disease (nvCJD, a human disorder related to Bovine spongiform encephalopathy), Gerstmann–Sträussler–Scheinker syndrome, fatal familial insomnia and kuru. These conditions form a spectrum of diseases with overlapping signs and symptoms." -Thank you Wikipaedia.
. A mutation at codon 178 of the prion protein gene causes a person to change over the next two weeks to two years into what sounds and stumbles like a zombie. The mutation replaces a hydrophyllic amino acid to a hydrophobic one. Likes water vs. hates water, super important. As a cell trait that is dominant this replacement prompts the propegation of dysfuctional cells to exponentially increase. The codon at 178 that gets replaced is Glutamic Acid (Molecular formula: C5H9NO4). It gets replaced by L-valine which in this example causes the cell indirectly to stop using the molecular building blocks it has stored up. Instead the effect is that the cellular purpose changes to one that reproduces (propagates) and resists deterioration. The understanding is similar to taking a fork in the road. As a result of resistance to digestion of building block proteins within the brain, what those brain cells need is not being given to them. Your brain cells can't fuel, they can not function and die of hunger and fatigue. Starve yourself of food or sleep for a few days and see what happens... (...seriously don't do that, 72 hours without sleep in some states is considered legally insane.)
. Where's the zombie apocalypse? If this thing can transmit by clay, despite outdoor exposure, let alone by consumption or by blood to blood transmission, and some think it could be sexually communicable; which it can, I'd be only a little concerned. If it has the ability to spread like that and you put a solid outbreak smack into the center of a less regulated society, we would be looking at infected areas where everyone is starting to stumble, loose sanity, coordination, balance, speech... Think about it...
However I don't see a reason to fear a now heavily monitored and regulated disease. Don't feed brain to what you eat and don't eat any brain. Most anything else is either uncontrollable or your fault.
. Your cells store up the ability to send messages (like feed me) through chemical naval bases. Need something, peel off a boat and send it off; the boat has "what's my address" instructions built into it and sometimes cells steal and propagate those instructions so that when one cell in the brain needs water, everyone up there gets some because the message's return address reads "brain." One of the instructions within the address bar includes a prion protein that directly impacts cell function. Normally this protein breaks up easily and provides certain chemicals to necessary processes to further operations. A diseased one refuses to break up and begins the process of sending itself to every near-by cell.
. The normal prion protein gene tells stored chemical and protein chains to break apart or digest easily. It normally travels and gets reproduced with any neurological chemical impulse. It also provides info on how often it should be copied. Which is wherever it goes to. There are instructions all along the chain of chemicals in storage saying where the edges are, start and stop. It's kind of like it comes with it's own instruction manual. A prion disease resists being broken down properly. Reminds me a little of cancer, aids and (oh yeah) zombies.
. Still too much of a jump? A dominant prion gene that tells the bonds in the storage portion of the cell to be hydro phobic means you display symptoms of extreme fatigue. No, I mean extreme. One gene that was found to be a natural carrier of this dominant protein later (in 1765) is called fatal familial insomnia. Remember L-valine, that's the evil one, the transmittable zombie disease is the L-valine protein replacement in the prion; well this one has another prion replacement that is so similar it's part of the same family. The interesting thing here is fatal familial insomnia (FFI) genetically inherited and alwa"ys caused by a mutation to the protein PrPC, but can also develop spontaneously in patients with a non-inherited mutation variant called sporadic Fatal Insomnia (sFI). FFI has no known cure and involves progressively worsening insomnia, which leads to hallucinations, delirium, and confusional states like that of dementia. The average survival span for patients diagnosed with FFI after the onset of symptoms is 18 months." -Wiki
. While you do get the dementia, poor vocal control, jerky often uncontrollable movements stiff gait or walk, lack of balance and coordination with altered memory and "psychosis" Symptoms lack a few key zombie characteristics. No peeling rotting skin, no intense hunger for brain (though there is something related to psychosis out there) and no undying. Gotta love that.
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