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Scientists have found a selective enzyme inhibitor that may be more effective than other painkillers with less side effects:
Pain and addiction have many biochemical roots, which makes it difficult to treat them without affecting other critical functions in cells. Today, the most potent painkillers are opioids, including heroin, oxycodone, and hydrocodone. In addition to interrupting pain, they inhibit enzymes known as adenylyl cyclases (ACs) that convert cells' energy currency, ATP, into a molecule involved in intracellular chemical communication known as cyclic AMP (cAMP). Chronic opioid use can make cells increase the activity of ACs to compensate, causing cAMP levels to skyrocket. When opioid users try to stop using, their cAMP levels remain high, and drugs that reduce those levels—like buprenorphine—have unwanted side effects.
A promising candidate for selectively reducing cAMP is one particular AC enzyme, known as AC1. Humans have 10 ACs, all of which convert ATP to cAMP. But they are expressed at different levels in different tissues, suggesting they serve disparate purposes. Over the last 15 years, experiments on mice without the gene for AC1 have shown they have reduced sensitivity to pain and fewer signs of opioid dependence. But the enzyme, along with its close relative AC8, also appears to be heavily involved in memory formation in a brain region known as the hippocampus. That could be bad news for a possible medicine that blocks AC1, says Val Watts, a pharmacologist at Purdue University in West Lafayette, Indiana. But the potential good news, he says, is that other animal studies suggest that the memory-forming work of AC1 and AC8 is redundant. So if AC1 is blocked selectively, it's likely to have only minimal effects on memory.
[...] Watts and his colleagues decided to set up a chemical test to screen a small group of compounds similar to forskolin, in search of one that inhibits AC1 but not AC8. That is just what they found [DOI: 10.1126/scisignal.aah5381] [DX], they report this month in Science Signaling. In cell-based studies, the compound, called ST034307, inhibits AC1 and reduces cAMP, while leaving AC8 unaffected. And when given to mice, it also reduces their sensitivity to pain.
(Score: 0) by Anonymous Coward on Thursday March 02 2017, @04:45PM (2 children)
It is just amazing the amount of BS you can produce via a string of null hypothesis tests and never making a single quantitative prediction or model. I have no idea about this research in particular, but am already 99.99% sure it will lead nowhere. It is a shame, since it doesn't need to be that way. Despite what will be claimed by lazy biomed researchers, it is a purely cultural problem:
https://bml.bioe.uic.edu/BML/Stuff/Stuff_files/biologist%20fix%20radio.pdf [uic.edu]
(Score: 0) by Anonymous Coward on Thursday March 02 2017, @04:49PM (1 child)
I forgot to include the current abstract for comparison:
Notice how everything is "inhibits" or "stimulated" or "enhanced". There are never numbers attached (and I bet if you tried to quantify their idea it would fall apart because it required insane reaction rates, concentrations, etc)
(Score: 0) by Anonymous Coward on Thursday March 02 2017, @07:01PM
Doesn't sound like something we can count on when we're facing prolonged torture sessions. Better stick with potassium cyanide [wired.com]!
(Score: 2, Insightful) by Ethanol-fueled on Friday March 03 2017, @02:31AM
It's kinda funny how the doctors started cracking down on prescriptions to "drug-seeking" opiate addicts just as all that CIA heroin from Afghanistan started flooding the markets. Gotta fund those black projects somehow.
it's like '70's Cambodia all over again! Air America!