Mephedrone -- A Popular Party Drug -- Could Help President Obama Get Re-Elected

Mephedrone was first synthesised in 1929, but did not become widely known until it was rediscovered in 2003. By 2007, mephedrone was reported to be available for sale on the internet... _Mephedrone, from Wikipedia

Mephedrone -- Wikipedia

US President Barack Obama faces the most difficult election challenge of his young career. Obama presides over an America that suffers a profound and worsening malaise, of a type not seen in the US since the late 1970s. From the worsening economy -- teetering on the brink of recession -- to deepening social divisions, Obama has given American voters very little rational reason to vote for him.

But voting is not necessarily a rational action, for most persons. In past elections, many people have voted a certain way in exchange for cigarettes or beer money. In fact, for many politicians, it would be better for voters to enter the polling booth in a deep stupour, with just enough wits to vote for the "right" person.

In extreme cases, you want to prepare voters well in advance of election day. Even an intoxicated person may retain enough inconvenient memories of a politician's incompetence and corruption, to vote against him even when besotted with intoxicants. Particularly bad leaders -- such as Obama -- will want to prepare ahead, by erasing bad memories of voters.

Unfortunately, it is not yet possible to selectively erase specific memories, so it would be necessary to destroy a broad memory spectrum, to ensure that the voter is unable to go against the instructions of his handler, once alone in the booth.

Fortunately, mephedrone -- a popular party drug -- may be exactly what Obama White House physicians ordered.

"You get the euphoria and touchy-feeliness of ecstasy together with the intense addictiveness of methamphetamine or cocaine," said Motbey.

...Rats were given an injection of mephedrone once a day for 10 days. The brains from one group of rats were examined an hour after their final dose. Another group of rats had several more weeks of drug-free living and were then given behavioural tests to find signs of long-term cognitive impairment, before their brains were also analysed.

"With this second group that lived drug free for an extended period we found a substantial memory impairment in animals that had been given the higher dose of the drug. This is concerning because it confirms earlier hints of memory problems in human mephedrone users. The fact the impairment was still there many weeks after the end of the drug treatment suggests that this damage may be permanent," said Motbey. _Mephedrone Brain Damage

Permanent brain damage from a party drug that makes you feel good and is addictive too? It may just work, for the unscrupulous incumbent who considers voters to be little better than laboratory rats.

Full PLOS mephedrone study

We know that convicted felons, drug abusers, and illegal aliens favour Obama (aka President Food Stamp) over his opponent by a very wide margin -- perhaps by as wide a margin as African Americans favour Obama.

By slipping mephedrone into municipal water supplies, and food suppliers such as Starbucks Coffees, and popular Ben & Jerry's ice cream, large portions of the US public could be made addicted to the drug unawares.

The sooner this covert campaign can be instituted, the earlier we should see the breaking down of unpleasant memories by American voters, and the sooner that Obama should start inching up in the opinion polls.

Obama may not quite be the absolute worst president the US has experienced. But already, he has created much hardship and many bad memories. Relying on the news media and educational system to dumb down US voters would probably take too long, in terms of the November election. A little more fast-acting help in the dumbing down department may be necessary.

This Is Your Brain Under General Anaesthesia

Neuroscience has often benefited from natural experiments—patients who lose their ability to remember, produce language, or regulate their emotions after parts of their brains are damaged or have to be surgically removed. Anesthesiologists preside over an analogous experiment every day: they watch elements of consciousness disappear. Under general anesthesia, for instance, patients lose pain perception, awareness, memory, and the ability to move. An anesthesiologist can influence each of these changes in different ways by varying the dosages and types of drugs used.

"By taking away different functions that we associate with consciousness," Brown says, "we might be able to start piecing together parts of the jigsaw puzzle." Neuroscientists could begin to do for consciousness what they have done with memory and language. _TechnologyReview

EEG Spectrum Under General Anaesthesia
Real time EEG monitoring is a useful adjunct to other ways of monitoring the anaesthetised patient. With better spatial resolution, EEG imaging of brain activity can make every surgical procedure a natural experiment in the mechanisms of consciousness.

EEG-based brain monitors are already a common sight in operating rooms; some anesthesiologists track the brain activity of their patients with commercially available monitors that use algorithms to transform EEG signals into crude indexes. (Others track only physical signs such as heart rate and blood oxygen levels.) But few of them, he says, spend time looking at the raw EEG data.

...As patients enter an anesthetized state, the normal pattern of low-intensity but high-frequency waves shifts to one of less frequent but more intense pulses—as if the constant chatter of the brain had given way to a chant. The location of activity shifts from the back of the brain to the front. Although it's possible to take patients into such a deep state of unconsciousness that their EEG is essentially flat, in most cases bursts of EEG activity alternate with periods of relative inactivity that can last for minutes. The brain processes appear "highly organized," he says. "There are very regular patterns in time, and very regular patterns in space."

...some drugs will decrease the frequency of brain waves seen in EEG readings, resulting in slow, regular oscillating waves across large areas of the brain. Other drugs cause certain areas to show fast, regular oscillations. Because anesthesiologists usually give a cocktail of drugs to each patient, these effects can happen simultaneously. The result, says Brown, is like a jammed signal: "Either way, [the different parts of the brain] can't communicate."

Over the past few years, other EEG studies have supported the idea that anesthesia doesn't simply shut the brain down but, rather, interferes with its internal communication. Mashour's research, for instance, has shown that feedback between the front and back of the brain is interrupted during general anesthesia, leading to a disconnect between different brain networks. That feedback is thought to be important for consciousness. _TechnologyReview

Clearly there are many ways to disrupt brain networks, and normal waking consciousness. Hypnosis has been used as "anaesthesia" during painful surgeries for over a hundred years. It will be fascinating to review the EEG pattern of such a surgery, for comparison to other anaesthetic agents.

We are still quite a long ways from developing the perfect anaesthetic, and from understanding human consciousness in all its states and varieties. But if western civilisation can hold up for just a few more decades against all of its internal and external enemies, some marvelous tools for enhanced health, cognition, longevity, and more, are on the way.

Why Do Antidepressants Take 6 Weeks to Work?

Until fairly recently, psychiatrists and neuropharmacologists have been puzzled by the several-week delay in onset of antidepressant efficacy of commonly prescribed mood elevators. It shouldn't take that long to boost neurotransmitter levels. But straight from central casting, the neural stem cell made its appearance in the science annals, and it was found that some antidepressants stimulate the differentiation of neural stem cells to mature nerve cells. Voila! New neurons--a feat once thought impossible!--from neural stem cells, with a little help from pharmacology. Recent work from the University of Texas supports that hypothesis.

...Antidepressants act very quickly to increase levels of natural compounds, called neurotransmitters, which nerve cells use to communicate. It takes several weeks to several months, however, for the patients who respond to such treatments to feel less depressed. Dr. Parada said this implies that some other long-term mechanism is also at work.

...Matching the timeframe for medicated patients to feel less depressed, it takes several weeks for new nerve cells to grow, Dr. Parada said. This parallel effect, he said, may mean that antidepressants need to stimulate growth of new cells in the dentate gyrus in order to achieve their full effect. _Sciencedaily

Antidepressants stimulate the production of new nerve cells in the hippocampus, and appear to protect nerve cells from apoptosis, at least in animal studies. The time delay for the mood elevation from antidepressants appears to be caused by the time to differentiation and integration of new neurons.

All this time, psychiatrists have been engaging in regenerative neuromedicine, and did not even realise it. Now that we have a better idea of what we are doing, perhaps we can learn to do it better?

Ampakine Update: S18986 and Brain Aging

Scientific work continues on the use of Ampakine drugs to treat Alzheimer's and other neurological disorders.

The drug, temporarily designated S18986, interacts with AMPA (short for α- Amino-3-hydroxy-5- methylisoxazole-4- propionic acid, or ampakine) receptors in the brain. These receptors transmit excitatory signals in the brain, and researchers were interested in experimental AMPA-receptor drugs (such as S18986) for their neuroprotective abilities and for the way they temporarily boost memory. But rather than investigating the compound’s short-term effects, Alfred E. Mirsky Professor Bruce McEwen and his lab members...studied the drug’s impacts on middle-aged to elderly rats and found that, when administered daily over four consecutive months, it appeared to improve memory and slow brain aging.

...When compared to control animals that had received only sugar water, the drugged rats were not only more active and better at memory tests, but their brains showed physical signs of slowed aging. Neurons in the forebrain that produce acetylcholine, a neurotransmitter known to play a role in learning and memory, had 37 percent less decline. Dopamine-producing neurons, which are responsible for sustaining activity and motivation levels, slowed their decline by 43 percent. Levels of inflammation in the brain were also significantly lower. “Every marker we chose to look at seemed to indicate there was some preservation of function during aging with chronic treatment,” Hunter says. The drug appears to slow aging’s effects throughout the entire brain.___ScienceDaily__via__FutureScanner

This particular Ampakine appears to have a protective effect on the brains of rats over a significant part of the rat's lifespan.

Ampakines are being researched as potential treatments for Alzheimer's, Depression, and other neuropathological and neuropsychiatric conditions. This research suggests an even broader potential application of Ampakines--as a neuroprotective for those at risk for neuropathology. Broadly speaking, that would be most of us, over our lifespans.

Wake Up! Hypocretin 1 Makes Sleep Optional

Orexin A (hypocretin-1) is a peptide hormone that according to recent research has the ability to keep monkeys awake. Now the US Military is attempting to show that it can do the same for humans.

Orexin A is a promising candidate to become a "sleep replacement" drug. For decades, stimulants have been used to combat sleepiness, but they can be addictive and often have side effects, including raising blood pressure or causing mood swings. The military, for example, administers amphetamines to pilots flying long distances, and has funded research into new drugs like the stimulant modafinil and orexin A in an effort to help troops stay awake with the fewest side effects.

...The research follows the discovery by Siegel that the absence of orexin A appears to cause narcolepsy. That finding pointed to a major role for the peptide's absence in causing sleepiness. It stood to reason that if the deficit of orexin A makes people sleepy, adding it back into the brain would reduce the effects, said Siegel....Any commercial treatment using the substance would need approval from the Food and Drug Administration, which can take more than a decade.Wired

What else can the orexins do besides help monkeys stay awake? Orexin reportedly also increases the craving for food.

Clearly there is a lot to be learned about the effects of these peptide hormones. This hormone has the potential to be a drug of abuse, if the FDA drags its feet too long.

Hat tip Impact Lab

Serotonin Receptor Agonists: Better than SSRI's?

Serotonin has been shown to be important in depression and anxiety. But what is the best "serotonin approach" to treating depression? SSRIs (selective serotonin reuptake inhibitors) such as Prozac are generally effective, but may take several weeks to achieve maximum effect. Another approach is for a drug to directly stimulate serotonin receptors--serotonin (5HT) agonists.

Recent research into 5HT4 receptor agonists, using rats as subjects, appears to promise faster and more efficacious serotonergic antidepressants.

Antidepressants that directly enhance serotonin signaling appear to have a much faster onset of action in animal models of depression than selective serotonin reuptake inhibitors (SSRIs), said investigators here.

Rats given one of two serotonin -- (HT4) agonists -- a new class of drug-showed behaviors and brain changes within three days that were suggestive of antidepressant effects that would take two to three weeks to achieve with an SSRI, reported Guillaume Lucas, Ph.D., of McGill University, and colleagues in the Sept 6 issue of Neuron.

The authors provide "and extensive and convincing data set" suggesting that this new class of molecules is fasting-acting and potentially efficacious, but whether they will see the light of day as therapies for human depression is still unknown, cautioned Ronald S. Duman, Ph.D., of Yale, in an accompanying editorial.

"These agents will require extensive testing in clinical trials for confirmation, because of limitations inherent in rodent models of depression and antidepressant response and because of potential side effects," Dr. Duman wrote.

Source

The important thing to remember is that although some humans may behave like rats, humans are not rats. Research on models of depression in rats may not transfer directly to good results in humans. Drug safety in humans and drug safety in rats are certainly not the same, either.

In an area of therapeutics such as depression, regulatory agencies will likely require extensive clinical studies before approval. It is important to point out, however, that depression is a potentially fatal disease. Any drug that promises rapid emergence from deep clinical depression, and which is also safe for short to intermediate term use, may find an important function in the treatment of depression--even if it is not approved for long term use.

This is an interesting result of the study:

They found that the action of the drugs on the 5-HT4 receptor "deeply modified" serotonin transmission by enhancing firing of dorsal raphe neurons in the hippocampus. In addition, three days of treatment also significantly promoted neurogenesis in the subgranular zone of the dentate gyrus of the hippocampus, an effect normally seen after a minimum of two weeks of treatment with classical antidepressants or SSRIs.

If depression kills neurons, and effective antidepressant therapy promotes new neuron growth, the new approach to stimulating serotonin receptors appears to do its formative work on neuronal stem cells more quickly than SSRIs.

Lily Is Looking at Possible "Prozac" of Antipsychotic Drugs

Drug companies such as Lilly are always looking for the "big score," like Lilly had with Prozac. Prozac was first in its class of the low side effect SSRI antidepressants, that largely replaced the more dangerous tricyclics and MAO inhibitors.

If results of a recent trial hold up, a new Lilly drug LY2140023 may be the prototype, first in its class, new anti-psychotic--without the troubling side effects of current anti-psychotics.

...According to the authors, the trial "provides strong new evidence for the role of glutamate modulation in treating psychosis, and specifically for mGlu2/3 receptor activation as a viable therapeutic approach to treat schizophrenia."

Crucially, LY2140023 has a very different adverse effect (AE) profile than the company's blockbuster antipsychotic Zyprexa (olanzapine), which had 2005 sales of over $4bn (€2.9bn).

Eli Lilly has been hit by a series of lawsuits over the side effects of olanzapine and has agreed to pay at least $1.2bn to 25,000 claimants.


...Most antipsychotic and atypical antipsychotic drugs, including olanzapine, work by affecting the dopamine and serotonin neurotransmitter pathways.

In contrast, LY2140023 works as a receptor agonist for the glutamate system, specifically targeting the metabotropic glutamate 2/3 (mGlu2/3) receptor to reduce the presynaptic release of the glutamate neurotransmitter in brain regions where mGlu2/3 receptors are expressed.

LY2140023 is a methionine amide oral pro-drug which is readily hydrolysed to form Eli Lilly's earlier candidate LY404039 which suffered from poor human oral absorption.

The trial, that included 196 patients suffering from schizophrenia, compared the effects of the new drug to placebo, as well as including olanzipine as an active control.

Treatment with LY2140023 was not observed to cause certain common AEs associated with schizophrenia treatments such as increased prolactin elevations, extrapyramidal symptoms and weight that occur with currently approved schizophrenia medications.

Drug Researcher

The target population for this drug would be schizophrenics and other psychotics. It is likely that other psychiatric and neurologic conditions will be amenable to mGlu2/3 receptor agonists, if the side effect profile is truly as advertised.

Only someone who has watched a schizophrenic recover much of his mental function on anti-psychotics, only to suffer from debilitating--even fatal--side effects from treatment, would appreciate the promise of a truly efficacious anti-psychotic with a benign side effect profile. If Lilly truly has come up with the "Prozac" of anti-psychotics, I wish them good fortune for it.

Important New Neuro-Research Tool--From the Sea

Experimental research in biology and pharmacology proceeds with the discovery of new research tools. Recently, University of Utah researchers discovered a new tool for research into an important neuroreceptor--the nicotinic Acetylcholine receptor. This receptor plays a critical role in the brain, muscle, and autonomic ganglia. This new tool promises to help find new treatments for neurological and neuromuscular diseases that currently cause large scale misery.

University of Utah researchers isolated an unusual nerve toxin in an ocean-dwelling snail, and say its ability to glom onto the brain's nicotine receptors may be useful for designing new drugs to treat a variety of psychiatric and brain diseases.

"We discovered a new toxin from a venomous cone snail that may enable scientists to more effectively develop medications for a wide range of nervous system disorders including Parkinson's disease, Alzheimer's disease, depression, nicotine addiction and perhaps even schizophrenia," says J. Michael McIntosh.

Discovery of the new cone snail toxin will be published Friday, Aug. 25 in The Journal of Biological Chemistry by a team led by McIntosh, a University of Utah research professor of biology, professor and research director of psychiatry, member of the Center for Peptide Neuropharmacology and member of The Brain Institute.

.... McIntosh says the OmIA toxin will be useful in designing new medicines because it fits like a key into certain lock-like "nicotinic acetylcholine receptors" found on nerve cells in the brain and the rest of the nervous system.

"Those are the same types of receptors you activate if you smoke a cigarette," he says, explaining that nicotine in cigarette smoke "binds" to the receptor to trigger the release of a neurotransmitter, which is a chemical that carries a nerve impulse from one nerve cell to another, allowing nerve cells to communicate.

"Nicotine acts on those receptors in our brain, but they are in our brain for better reasons than to enjoy a cigarette," McIntosh says. Different forms or subtypes of nicotinic receptors control the release of different neurotransmitters. "That's important because if you had compounds to facilitate the release of one neurotransmitter and not another neurotransmitter, that opens up medicinal potential," he says.

"For instance, one receptor modifies the release of dopamine. There are inadequate amounts of dopamine in Parkinson's disease," so a medicine designed to fit into a certain subtype of nicotinic receptor would produce more dopamine and thus protect against the development of tremors and other Parkinson's symptoms. Indeed, other studies have found that smoking seems to forestall Parkinson's disease.

A medicine that could block certain nicotinic receptors could be used to help people stop smoking cigarettes, and the same method might work for alcoholism because nicotinic receptors may be involved in alcohol addiction, McIntosh says.

Other nicotinic receptors trigger the release of neurotransmitters involved in memory, so activating the right receptors might lessen Alzheimer's memory loss.

"One reason people smoke is they feel their thinking may be a little better, with increased attention and focus," McIntosh says, noting that pharmaceutical companies "would like to mimic that positive benefit without all the downsides of cigarette smoke."

Other nicotinic receptors influence "the release of serotonin and norepinephrine, two neurotransmitters strongly implicated in mood disorders" such as depression, so a drug to activate those receptors might treat depression, he adds.

Schizophrenics tend to smoke heavily because something in cigarette smoke "seems to help them filter out irrelevant stimuli. They can focus better," McIntosh says. So a drug aimed at certain nicotinic receptors might treat schizophrenia.

....he snails from which the new toxin was obtained were collected by divers in Olivera's native Philippines. Venomous snails use a dart-like tooth to zap fish, snails and other prey, injecting them with an immobilizing toxin. Venom from the collected snails was extracted at a lab in the Philippines, and then sent to Utah.

Once the screening process identified OmIA as promising, McIntosh and colleagues purified the toxin – one of perhaps 200 components in Conus omaria venom. They determined its chemical structure and then synthesized more of the toxin, since they had only a small amount of the natural version.

Next, the synthetic toxin was tested to see how well it acted as a "key" to fit into the "locks" represented both by binding proteins (from freshwater snails and a sea slug) and by actual nicotinic receptors, which came from rat cells but were grown in frog eggs. That allowed the researcher to grow various subtypes of the nicotinic receptors and see how well the toxin fit them.

Taylor and Han provided pictures of the physical structures of the binding protein "locks" and toxin "key," and then "used computer simulation to dock the two structures together," says McIntosh. "That generates a picture of the binding site – the points of contact between the toxin and the binding protein."

The site is the place a new drug would be designed to fit.

"The whole idea is to make the model of the nicotinic receptor so predictive that you can then really speed up the development of drugs," McIntosh says. "If you have an accurate model of the receptor, you can plug in a model of your drugs and do a lot of 'virtual screening.' Rather than synthesizing a million compounds and having all but one be duds, you can synthesize a few thousand compounds based on the model and come up with a better drug with less time and resources."

Source.

It is nice to find new drugs, and new classes of drugs, from nature. Finding a new research tool is even better, since new research tools can lead to new drugs, new classes of drugs, even new approaches to an entire field of study.

Smart Drugs: What are the Prospects?

We begin with an article from Sciam Mind, by Michael Gazzaniga.
Enhancing intelligence is not science fiction. Many "smart" drugs are in clinical trials and could be on the market in less than five years. Some medications currently available to patients with memory disorders may also increase intelligence in the healthy population. Likewise, few people would lament the use of such aids to ameliorate the forgetfulness that aging brings. Drugs that counter these deficits would be adopted gratefully by millions of people.

Drugs designed for psychotherapy can also be used to enhance certain regular mental functions. Just as Ritalin can improve the academic performance of hyperactive children, it can do the same for normal children. It is commonly thought to boost SAT scores by more than 100 points, for both the hyperactive and the normal user. Many healthy young people now use it that way for that purpose, and quite frankly, there is no stopping this abuse.

... consider the following. In July 2002 Jerome Yesavage and his colleagues at Stanford University discovered that donepezil, a drug approved by the FDA to slow the memory loss of Alzheimer's patients, improves the memory of the normal population. The researchers trained pilots in a flight simulator to perform specific maneuvers and to respond to emergencies that developed during their mock flight, after giving half the pilots donepezil and half a placebo. One month later they retested the pilots and found that those who had taken the donepezil remembered their training better, as shown by improved performance. The possibility exists that donepezil could become a Ritalin for college students. I believe nothing can stop this trend, either.

...Recently geneticists have discovered that even such abstract qualities as personality and intelligence are coded for in our genetic blueprint. Studies of the genetic basis of g are just beginning, and because g most likely arises from the influence of many genes, the hunt will be a long one. Yet one study has already found that a gene on chromosome 6 is linked to intelligence.

So-called genetic brain mapping could help the search. Scientists are looking at the structural features (size, volume, and so on) of the brains of many individuals, including twins, familial relatives and unrelated individuals. By scanning all these brains in magnetic resonance imaging machines and looking at the differences, researchers have been able to determine which areas of the brain are most under the control of genes. These studies have emerged only in the past three to four years. Geneticists hope that once they know which brain areas are most affected by heredity, they can figure out which genes are responsible for those regions. With this kind of reverse mapping, the experts should be able to learn more about the genetics of intelligence.

...Whatever happens, we can be sure that cognitive enhancement drugs will be developed and that they will be used and misused. But just as most people do not choose to alter their mood with Prozac and just as we all reorient our lives in the face of unending opportunities to change our sense of normal, our society will absorb new memory drugs according to each individual's underlying philosophy and sense of self. Self-regulation will occur. The few people who desire altered states will find the means, and those who do not want to alter their sense of who they are will ignore the drug potions. The government should stay out of it, letting our own ethical and moral sense guide us through the new enhancement landscape. by Michael Gazzaniga

Next we go to Nootropics.com, a Hedweb site. This review of "Smart Drugs 2" by John Morgenthaler and Steven Fowkes, links to discussions of several potential smart drugs, as well as discussions about the underlying neuroscience and pharmacology involved. Here, we are introduced to modafinil, an increasingly prescribed drug that seems to do what it is supposed to do, with few serious side effects.

Modafinil, or Provigil, is a new stimulant with several different indications, and many more off label uses. Modafinil.org lists 45 uses of modafinil, cognitive enhancement being number 45. Modafinil.com is another Hedweb site, full of links to other pages describing the neuropharmacology of provigil, and the underlying neuroscience involved. Modafinil is becoming very popular with young professionals who never seem to have enough time to get everything done. Militaries use it for special ops troops, helicopter pilots, and pilots on long bombing missions. It works for ADD/ADHD, as an adjunct for depression, for cerebral palsy, and many more dysfunctions. Cephalon is coming out with a single isomer formulation of modafinil called "Nuvigil."

Both donazepil and modafinil are available from physicians, and over the internet. The ethics of internet prescribing are a bit shaky, but expect these drugs to become more available, rather than less, with time.

The last stop on today's smart drug train is the Ampakine station. Ampakines have the potential to not only help normal people think more clearly, as Donazepil and Modafinil seem to do, but to also make them "smarter." Ampakines directly affect the basic learning system of the brain.

New Scientist presented an article last May titled "11 Steps to a Better Brain." Gary Lynch, the inventor of ampakines, was cautious but optimistic:
The drug acts only in the brain, claims Lynch. It has a short half-life of hours. Ampakines have been shown to restore function to severely sleep-deprived monkeys that would otherwise perform poorly. Preliminary studies in humans are just as exciting. You could make an elderly person perform like a much younger person, he says.

While donazepil works on the acetylcholine system, and modafinil works on dopamine receptors, ampakines in contrast affect the glutamate receptors, specifically AMPA receptors. From neurotrasmitter.net, here are a few dozen scientific abstracts dealing with potential ampakines and mechanisms of ampakines--if the wikipedia article did not give you enough information.

That is a lot of information to digest, although if you take these drugs it may not be as difficult as you might think. Perhaps a joke, perhaps not? In time, people who choose not to boost their cognition may be less common than those who choose to do so.

The long term goal is to adjust the genes themselves, to do a better job of improving cognition than any one drug, or symphony of drugs, could possibly do. In the meantime, expect smart drugs to be delivered by pill, injection, skin patch, long term implant, and even injector pumps. The intelligence of a population is serious business, more serious than most people understand. For now.

Another Anti-Alzheimer's Compound

This bio.com newsfeature points to research done at Northwestern University.

As described in the Jan. 11 issue of the Journal of Neuroscience, the compound, called MW01-5-188WH, selectively inhibits production of pro-inflammatory proteins called cytokines by glia, important cells of the central nervous system that normally help the body mount a response, but are overactivated in certain neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, stroke and traumatic brain injury.

The compound was designed and synthesized in the laboratory of D. Martin Watterson at Northwestern University Feinberg School of Medicine, using a synthetic chemistry platform developed in his lab by researchers at the Northwestern University Center for Drug Discovery and Chemical Biology (CDDCB) for the rapid discovery of new potential therapeutic compounds.

Watterson is co-director of the CDDCB, the J.G. Searle Professor of Molecular Biology and Biochemistry and professor of molecular pharmacology and biological chemistry at the Feinberg School.

There is a delicate balance of pro-inflammatory and anti-inflammatory hormones, including cytokines, in the neuron's environment. Rational drug design methods allow the targeted development of chemical compounds designed for very specific purposes. These compounds are not necessarily safe and effective because they were "rationally designed." They must still go through a thorough vetting process by national drug regulatory agencies. But even if these pinpoint specific compounds fail the tests for regulatory approval, they are often still useful scientific probes for studying biological systems. Development of these rapid discovery tools is one of many new mechanisms propelling biological science rapidly ahead.