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March 3rd, 2012 
FAKE NEWS for the Zionist agenda Photo illustration: Curtis Mann; Photo: Ed Andrieski/AP
Recoveries are possible, but they aren’t necessarily neat. One of Brunet’s patients was Lois, a retired member of the Canadian military living in Kingston, Ontario. (She asked that I not use her last name.) When Lois describes the tragic arc of her life, she sounds like a cursed character in the Old Testament. Sexually molested as a child, she married an abusive man, who would later hang himself at home. Years after that, her teenage daughter was hit by a truck and died. “I’d been holding it together my entire life,” she says. “But when I heard my child was gone I just started sobbing and couldn’t stop. I felt this pain that I thought was going to kill me.”
Lois coped by drinking. She would start around noon and keep going until she went to bed. “I lost four years to alcohol,” she says. “But if I wasn’t drunk then I was crying. I knew I was killing myself, but I didn’t know what else to do.”
In early 2011, Lois learned about the experimental trials being conducted by Brunet. She immediately wrote him an email, begging for help. “I’d spent a lot of my life in standard talk therapy,” she says. “It just didn’t do it for me. But this seemed like it might actually work.” Last spring Lois began reconsolidation treatment at Brunet’s hospital, driving to Montreal once a week. The routine was always the same: A nurse would give her propranolol, wait for the drug to take effect, and then have her read her life story out loud. The first few weeks were excruciating. “I was a mess for days afterward,” she says. “I couldn’t believe I’d signed up for this.” But then, after five weeks of therapy, Lois felt herself slowly improve. She would still cry when describing the death of her daughter—Lois cried during our interview—but now she could stop crying. “That was the difference,” she says. “I still remembered everything that happened, and it still hurt so much, but now I felt like I could live with it. The feelings were just less intense. The therapy let me breathe.”
Such improvements, small though they may seem, are almost unheard of in psychiatry. “We never cure anything,” Brunet says. “All we do is try to treat the worst symptoms. But I think this treatment has the potential to be the first psychiatric cure ever. For many people, the PTSD really is gone.”
Propranolol, of course, is an imperfect drug, a vintage tool commandeered for a new purpose. Despite Brunet’s optimistic assessment, many of his patients remain traumatized, albeit perhaps less so. While he is currently conducting a larger-scale, randomized PTSD trial with the beta-blocker, future therapies will rely on more targeted compounds. “These norepinephrine inhibitors are just what’s available right now,” LeDoux says. “They work OK, but their effect is indirect.” What reconsolidation therapy really needs is a drug that can target the fear memory itself. “The perfect drug wouldn’t just tamp down the traumatic feeling,” he says. “It would erase the actual representation of the trauma in the brain.”
Here’s the amazing part: The perfect drug may have already been found.
The chemistry of the brain is in constant flux, with the typical neural protein lasting anywhere from two weeks to a few months before it breaks down or gets reabsorbed. How then do some of our memories seem to last forever? It’s as if they are sturdier than the mind itself. Scientists have narrowed down the list of molecules that seem essential to the creation of long-term memory—sea slugs and mice without these compounds are total amnesiacs—but until recently nobody knew how they worked.
In the 1980s, a Columbia University neurologist named Todd Sacktor became obsessed with this mental mystery. His breakthrough came from an unlikely source. “My dad was a biochemist,” Sacktor says. “He was the one who said I should look into this molecule, because it seems to have some neat properties.” Sacktor’s father had suggested a molecule called protein kinase C, an enzyme turned on by surges of calcium ions in the brain. “This enzyme seemed to have a bunch of properties necessary to be a regulator of long-term potentiation,” Sacktor says. “But so did a bunch of other molecules. It took me a few years to figure out if my dad was right.”
In fact, it took Sacktor more than a decade. (He spent three years just trying to purify the molecule.) What he discovered is that a form of protein kinase C called PKMzeta hangs around synapses, the junctions where neurons connect, for an unusually long time. And without it, stable recollections start to disappear. While scientists like Nader had erased memories using chemicals that inhibited all protein synthesis, Sacktor was the first to target a single memory protein so specifically. The trick was finding a chemical that inhibited PKMzeta activity. “It turned out to be remarkably easy,” Sacktor says. “All we had to do was order this inhibitor compound from the chemical catalog and then give it to the animals. You could watch them forget.”
What does PKMzeta do? The molecule’s crucial trick is that it increases the density of a particular type of sensor called an AMPA receptor on the outside of a neuron. It’s an ion channel, a gateway to the interior of a cell that, when opened, makes it easier for adjacent cells to excite one another. (While neurons are normally shy strangers, struggling to interact, PKMzeta turns them into intimate friends, happy to exchange all sorts of incidental information.) This process requires constant upkeep—every long-term memory is always on the verge of vanishing. As a result, even a brief interruption of PKMzeta activity can dismantle the function of a steadfast circuit.
If the genetic expression of PKMzeta is amped up—by, say, genetically engineering rats to overproduce the stuff—they become mnemonic freaks, able to convert even the most mundane events into long-term memory. (Their performance on a standard test of recall is nearly double that of normal animals.) Furthermore, once neurons begin producing PKMzeta, the protein tends to linger, marking the neural connection as a memory. “The molecules themselves are always changing, but the high level of PKMzeta stays constant,” Sacktor says. “That’s what makes the endurance of the memory possible.”
For example, in a recent experiment, Sacktor and scientists at the Weizmann Institute of Science trained rats to associate the taste of saccharin with nausea (thanks to an injection of lithium). After just a few trials, the rats began studiously avoiding the artificial sweetener. All it took was a single injection of a PKMzeta inhibitor called zeta-interacting protein, or ZIP, before the rats forgot all about their aversion. The rats went back to guzzling down the stuff.
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