just wanted to comment on this body can fix itself
Post# of 30029
Posted On: 02/09/2015 1:45:15 AM
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just wanted to comment on this body can fix itself Alzheimers USC study as it pertains to MANF and the recently published chinese/baltimore research on inflammation
http://www.cell.com/neuron/abstract/S0896-6273(14)01201-X
http://www.nature.com/srep/2015/150202/srep08...33_F5.html
If blocking interleukin 10 (IL-10) is good for ALZ (which I can't read the full article, so I don't know what mechanisms they're specifying), then I have a hard time seein MANF as ultimately helpful for ALZ and here's why:
Let’s start at the top. We’re talking about inflammation. You know, the kind you get when you get arthritis, when House correctly identifies you as having Lupus, when you hurt your joints. Inflammation is theorized to underlie a great many diseases, including ALZ, PD actually I’ll stop, it’s a part of almost any disease worth mentioning, and is a fundamental aspect of biology. It is one of the body’s basic responses when shit goes down, e.g. when a pathogen enters the body, when cells get damage (head trauma anyone?), when you brush against poison ivy etc. Sometimes our body can overreact, react proactively, and sometimes our body just screws up and misfires. That’s kind of what we’re talking about here.
Amarantus is all about endoplasmic reticulum stress and the cell cycle getting messed up/junked up because of misfires. The MANF article, and the article that said the body could fix itself via interleukin 10 (IL10) suppression are all about signaling pathways getting messed up and correcting those. Both IL-10 and MANF can play a key role in an inflammation pathway around TNFa and nfkB.
What's the bio: TNF-α (tumor necrosis factor alpha tnfa) is one of several pro-inflammatory cytokines (proteins involved in cell signaling) that are suppressed by IL-10 (interleukin 10) through the inhibition on the transcription factor nf-kB (nuclear factor kappa
. When tnfa gets into certain parts of the Endoplasmic reticulum it changes a few specific receptors and sets off a chemical chain reaction, one of the consequences of which can be nfkb activation. nfkb normally can’t translocate/activate, but when tnfa sets off that chemical reaction, a protein(Ikb) that basically holds nfkb back gets zapped by an enzyme. Nfkb, upon translocation to the cell nucleus, attaches itself to sections of genes called promoters that lead to the production of proteins and other shit that lead to inflammation. That same inhibitory protein(Ikb) that needs to get zapped in reaction that releases nfkb gets shielded by IL10 (and in fact nfkb is made up of two clumps of shit p50 and p65, and only one of the clumps(p50) breaks off/activates/translocates to nucleus when IL10 is involved. So IL10 blocks p65 translocation.) Alternately, MANF does not inhibit p65 translocation, but it DOES prevent p65 binding to the genes in the nucleus after translocation that lead to the creation of inflammatory bullshit proteins etc. MANF doesn’t mess with ikb at all, but you get the same end result TNF-a induced nfkb inflammation is suppressed. The proteins made from the genes that need p65 to attach never get made and never cause inflammation.
MANF and IL-10 regulate inflammation in a very similar way. If cell cycle is the ALZ hypothesis, I simply cannot see how more MANF but less IL-10 would make sense. But who knows. As a caveat, something to note for both of these studies, which were done on mice, not humans, is that TNFa/TNF among other proteins are not biologically conserved in structure. Also, this is a summary of a super complicated process that is clearly involved in so much cross talk inside a cell, God knows how it all works out in its entirety. It’s just hard to take any good news from that recent MANF inflammation article with regards to an ALZ treatment if the USC study is true. I see no way in which MANF would reduce IL10, and it appears to have similar affects.
Still long, yes like I said I did double down my shares last week off my tax return. MANF clearly still plays incredibly active roles in human biology which will be elucidated if not commercialized one day. Please, for other board members scientifically inclined, educate me further. I merely hold a degree in chemistry, I’m no doctor.
http://www.cell.com/neuron/abstract/S0896-6273(14)01201-X
http://www.nature.com/srep/2015/150202/srep08...33_F5.html
If blocking interleukin 10 (IL-10) is good for ALZ (which I can't read the full article, so I don't know what mechanisms they're specifying), then I have a hard time seein MANF as ultimately helpful for ALZ and here's why:
Let’s start at the top. We’re talking about inflammation. You know, the kind you get when you get arthritis, when House correctly identifies you as having Lupus, when you hurt your joints. Inflammation is theorized to underlie a great many diseases, including ALZ, PD actually I’ll stop, it’s a part of almost any disease worth mentioning, and is a fundamental aspect of biology. It is one of the body’s basic responses when shit goes down, e.g. when a pathogen enters the body, when cells get damage (head trauma anyone?), when you brush against poison ivy etc. Sometimes our body can overreact, react proactively, and sometimes our body just screws up and misfires. That’s kind of what we’re talking about here.
Amarantus is all about endoplasmic reticulum stress and the cell cycle getting messed up/junked up because of misfires. The MANF article, and the article that said the body could fix itself via interleukin 10 (IL10) suppression are all about signaling pathways getting messed up and correcting those. Both IL-10 and MANF can play a key role in an inflammation pathway around TNFa and nfkB.
What's the bio: TNF-α (tumor necrosis factor alpha tnfa) is one of several pro-inflammatory cytokines (proteins involved in cell signaling) that are suppressed by IL-10 (interleukin 10) through the inhibition on the transcription factor nf-kB (nuclear factor kappa
. When tnfa gets into certain parts of the Endoplasmic reticulum it changes a few specific receptors and sets off a chemical chain reaction, one of the consequences of which can be nfkb activation. nfkb normally can’t translocate/activate, but when tnfa sets off that chemical reaction, a protein(Ikb) that basically holds nfkb back gets zapped by an enzyme. Nfkb, upon translocation to the cell nucleus, attaches itself to sections of genes called promoters that lead to the production of proteins and other shit that lead to inflammation. That same inhibitory protein(Ikb) that needs to get zapped in reaction that releases nfkb gets shielded by IL10 (and in fact nfkb is made up of two clumps of shit p50 and p65, and only one of the clumps(p50) breaks off/activates/translocates to nucleus when IL10 is involved. So IL10 blocks p65 translocation.) Alternately, MANF does not inhibit p65 translocation, but it DOES prevent p65 binding to the genes in the nucleus after translocation that lead to the creation of inflammatory bullshit proteins etc. MANF doesn’t mess with ikb at all, but you get the same end result TNF-a induced nfkb inflammation is suppressed. The proteins made from the genes that need p65 to attach never get made and never cause inflammation. MANF and IL-10 regulate inflammation in a very similar way. If cell cycle is the ALZ hypothesis, I simply cannot see how more MANF but less IL-10 would make sense. But who knows. As a caveat, something to note for both of these studies, which were done on mice, not humans, is that TNFa/TNF among other proteins are not biologically conserved in structure. Also, this is a summary of a super complicated process that is clearly involved in so much cross talk inside a cell, God knows how it all works out in its entirety. It’s just hard to take any good news from that recent MANF inflammation article with regards to an ALZ treatment if the USC study is true. I see no way in which MANF would reduce IL10, and it appears to have similar affects.
Still long, yes like I said I did double down my shares last week off my tax return. MANF clearly still plays incredibly active roles in human biology which will be elucidated if not commercialized one day. Please, for other board members scientifically inclined, educate me further. I merely hold a degree in chemistry, I’m no doctor.
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