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This blog relates science with an emphasis on neuroscience to every day topics and events.
Lisa Conti
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- September 29, 2008
- 06:58 PM
- 677 views
The Last Pop Stop: Popcorn, FAT and the brain
by Lisa Conti in Stimulating Aliquot
It started with a conversation about popcorn. My husband and the neighbor share a love for it. But my husband has another gustatory indulgence, bacon. Combined with his tendency for wild exaggeration and his knack for persuasion, he convinced the neighbor that uniting the two foods occurred in kitchens routinely. “I pop it in bacon grease, doesn't everyone!” was what he told her.What exactly happens when fat hits the tongue? Rather, when it melts onto it, mixing with saliva while not dissolving in it, creeping its way into the furrows and between the taste buds. Is it the flavor, the texture or the ability of the lipid to carry smell, that tickles the mouth in such a way to warrant taking another bite and another and another?Up until a couple of years ago, scientists would argue that our tongue likes to wallow in fat's creaminess, leaving flavor for sweet, salty, sour and savory (umami) receptors to sense. But in 2005, a protein lodged in the tips of taste cells (in mice) was found to recognize fat.Each taste bud, containing 50 to 100 taste cells extend into tiny wispy structures, feelers, reaching into the world of the mouth. Taste receptors—proteins—are tucked into the cell like sausages baked in pastries. Slathered in saliva, they await their signal.Experiments show that when mice are given a fatty mouthful, the liver and pancreas release digestive secretions even when the fat never exits the mouth. The protein described three years ago as the tongue's fat detector, ironically called FAT (standing for Fatty Acid Transporter) is thought to signal through nerve cells, telling the gut by way of the brain, that fat is on the way. But, the brain does more than to communicate with viscera. Neurotransmitters such as endorphins, released soon after fat intake, transmit feel good signals.This burgeoning FAT research is lead by a group in France—a place where fat infused cuisine is emblematic. And the research team's latest results are the most mouth watering: that fat has “taste”. Monitoring the inside of mouse taste cells, the scientists noted a “taste” signature—a molecule that was released only when the cell was exposed to fat. They also established that a nerve bridging the mouth to the brain conveys this taste signal and associate a region in the brain involved in tasting. This distinction is notable. Until now, report after report states fat is flavorless. The authors conclude that “The gustatory pathway is involved in the oral perception of long chain fatty acids in the mouse.”But what about for humans. Without evidence that the FAT protein is present in my taste cells, I have to wonder if fat has real flavor? When a mouse eats triglycerides (found in animal fat) an enzyme (in saliva) breaks them down into fatty acids. This process, however, has not been described in people. And it hasn't been shown that the FAT protein is in our taste buds.Inspired by the popcorn discussion, our neighbor went home and cooked two slices of bacon. She saved the fat and later that night fortified the vegetable oil she normally uses to make popcorn. She raved about the product well before she discovered my husbands lack of candor.I have endured many popcorn experiments. Popcorn popped in coconut oil, in corn oil, popcorn scorched in butter, popped with sugar, bathed in butter, air popped, shaken on the stove top, popped in aluminum and stainless steal poppers. Bacon grease is the last pop stop.The experience my neighbor reported included a combination of flavor and olfactory sensations that sounded exquisitely synergistic. Now it was time to do my own experiment and I couldn't have timed it better. Last night we had a house full of vegetarians (all with a well developed sense of humor). The potluck included: baked potatoes, grated cheese, green beans, rice, pasta with red sauce, bread, bruschetta and... bacon. After dinner, we gathered in the living room to watch surfing and Tuvan throat singing documentaries and to eat, lard popped pop corn.Going into the experiment, I was skeptical. Especially since, our popping agent was not diluted with vegetable oil. I imagined a thick film would coat my tongue and the roof of my mouth. And projected that translucent sheen eventually transferring to the inner walls of my arteries to form a thick yellow/white layer. But I have to say, the palatability was indeed superb and surprisingly light. Salty, savory—satisfying, despite my bias. Handful after handful found their way to mouths and soon it was gone.Now, I'm sure there are a few other reasons why this popcorn was particularly delicious. After all, it contains almost every other taste stimulator. Protein remnants surely activated savory receptors. Every bite was a miniature salt explosions. And the tongue's sweet sensors couldn't be silent as saliva induces breakdown of starchy corn. Oh, the aroma too. As my neighbor put it, “It's a real delicacy. Though, sprinkling it with cheddar cheese might even make it better.”And so the popcorn conversation spurred not only my interest in what makes fat good but what makes the perfect bowl of popcorn. I'll have to keep you posted on the science behind the flavor of fat but I will tell you an excellent popcorn recipe that doesn't require lard:2 Tablespoons grape seed oil2 Tablespoons butterHeat in a stainless steal popper with a turn paddle. Add¼ cup popcornD. Gaillard, F. Laugerette, N. Darcel, A. El-Yassimi, P. Passilly-Degrace, A. Hichami, N. A. Khan, J.-P. Montmayeur, P. Besnard (2007). The gustatory pathway is involved in CD36-mediated orosensory perception of long-chain fatty acids in the mouse The FASEB Journal, 22 (5), 1458-1468 DOI: 10.1096/fj.07-8415com... Read more »
D. Gaillard, F. Laugerette, N. Darcel, A. El-Yassimi, P. Passilly-Degrace, A. Hichami, N. A. Khan, J.-P. Montmayeur, & P. Besnard. (2007) The gustatory pathway is involved in CD36-mediated orosensory perception of long-chain fatty acids in the mouse. The FASEB Journal, 22(5), 1458-1468. DOI: 10.1096/fj.07-8415com
- July 31, 2008
- 06:15 PM
- 531 views
Hand in Hand
by Lisa Conti in Stimulating Aliquot
In my recent endeavor to cut back on paper consumption, I've converted bank statements to digital versions, put a stop to mail catalogs, and have been doing most of my reading and writing online.Speaking of, I've also been writing for www.Miller-McCune.com including their blog Today in Mice -check it if you like the kind of stuff you're reading here. But I diverge, the real issue that I'm blogging about today goes with reading/writing on the computer.There's one bit of paper that I can't eliminate from my life -it's the writing that I do while I read science. At first I thought it was just a habit, scribbling notes and flow charts in the margins of scientific papers. But when I keep notes on the computer, without pen in hand, the information seems to trickle away like a lost train of thought.A recent study published in the Journal of Cognitive Neuroscience suggests that it may be better to learn by writing (with your hand that is). In other words, learning and motor function go hand in hand.Scientists from the Universite Paul Sabatier, the Universite de La Mediterranee and the Hopital de La Timone in France primarily interested in how we learn characters or symbols for written language, gave twelve subjects new characters to learn -either by handwriting or typing them. When tested, the individuals remembered the the funny lines and loop-d-loops and their orientation best when they were practiced by handwriting. Using motor skills to hit a key -even though the time spent on the task was equivalent- didn't cut it.One intriguing aspect of the study is that the researchers used brain imaging to compare the neural pathways involved in both processes. Broca's area, historically associated with speech, is gaining recognition for a more broad role in language. The authors discern that the “left Broca's area activation seems to depend on the motor knowledge associated with the characters.”This research is directly relevant to children learning to write. My preschool aged daughter, obsessed with the computer, sees me typing and wants to do her writing too. Letting her practice her letters with enlarged fuschia-font, I used to feel pretty good about the exercise. While the activity is not detrimental, I now make an extra effort to have her put in sufficient time with paper and pencil.Taking the research to the level of comprehension may be speculative but the direct implications of this study and my anecdotal evidence is keeping paper in our lives.Longcamp, M., Boucard, C., Gilhodes, J., Anton, J., Roth, M., Nazarian, B., Velay, J. (2008). Learning through Hand- or Typewriting Influences Visual Recognition of New Graphic Shapes: Behavioral and Functional Imaging Evidence. Journal of Cognitive Neuroscience, 20(5), 802-815. DOI: 10.1162/jocn.2008.20504... Read more »
Marieke Longcamp, Céline Boucard, Jean-Claude Gilhodes, Jean-Luc Anton, Muriel Roth, Bruno Nazarian, & Jean-Luc Velay. (2008) Learning through Hand- or Typewriting Influences Visual Recognition of New Graphic Shapes: Behavioral and Functional Imaging Evidence. Journal of Cognitive Neuroscience, 20(5), 802-815. DOI: 10.1162/jocn.2008.20504
- June 27, 2008
- 08:55 PM
- 728 views
Sea Lions Suffer
by Lisa Conti in Stimulating Aliquot
Since I frequent the same California beaches weekly, I can't help but keep tabs on the big things that wash up. The picture above is of a decaying sea lion. My friend pointed it out about a week before the photo was taken. At that point the animal was alive and exhibiting a behavior she called “the Stevie Wonder”. Swaying his head back and forth, it was clear the animal wasn't well.These days, this isn't an unusual sight. There are many sick or decaying seals and sea lions on the beach. Many of them sway, wallow and make their way, eventually, back to “health”. The cause: domoic acid, a neurotoxic product of what's called an algal bloom. These harmful blooms are increasing and the marine mammals are suffering.A report published in the Proceedings of The Royal Society B (February 2008) shows that domoic acid exposed sea lions are developing a chronic condition. Researchers from several agencies including California's Public Health and the National Oceans Services examined hundreds of sea lions suffering from domoic acid poisoning over the last ten years.What they've noticed is that, aside from initial acute symptoms, the animals may develop a “chronic epileptic syndrome characterized by behavioral changes, seizures and atrophy of the hippocampal formation.” They become lazy, vomit and twitch.The results section of the paper references specific cases of strange activities. “Abnormal behaviors included standing in atypical locations (sleeping in a public restroom, climbing onto police cars, found up to 100 miles inland in an artichoke field, car dealership or walking down the road).”On the upside, the authors conclude that these sick animals may provide a good model for human epilepsy and also serve as a tell tale for dangerous seafood.On the downside, as the algal booms increase, marine mammals are likely to suffer more -and if the upside is knowing when our food is bad, the obvious negative is the potential of domoic acid poisoning for you and me.Goldstein, T., Mazet, J., Zabka, T., Langlois, G., Colegrove, K., Silver, M., Bargu, S., Van Dolah, F., Leighfield, T., Conrad, P., Barakos, J., Williams, D., Dennison, S., Haulena, M., Gulland, F. (2007). Novel symptomatology and changing epidemiology of domoic acid toxicosis in California sea lions (Zalophus californianus): an increasing risk to marine mammal health. Proceedings of the Royal Society B: Biological Sciences, 275(1632), 267-276. DOI: 10.1098/rspb.2007.1221... Read more »
T Goldstein, JAK Mazet, TS Zabka, G Langlois, KM Colegrove, M Silver, S Bargu, F Van Dolah, T Leighfield, PA Conrad.... (2007) Novel symptomatology and changing epidemiology of domoic acid toxicosis in California sea lions (Zalophus californianus): an increasing risk to marine mammal health. Proceedings of the Royal Society B: Biological Sciences, 275(1632), 267-276. DOI: 10.1098/rspb.2007.1221
- May 28, 2008
- 10:38 AM
- 540 views
Your Memory Is In Your Blood
by Lisa Conti in Stimulating Aliquot
I was two thirds of the way to the end of a 45 member circle at a workshop, hating my position in the line-up. The facilitator started an introduction exercise that involved reciting the names of preceding individuals -from the beginning. The room was filled with science types, many commenting on the cognitive process of memory. As the people before me went, I concentrated on the names, faces and associating ideas with them. Dawn had an image of the rising sun behind her dark hair and Robin's pale blue blouse was like an egg.The blood flowing through our veins is packed with cells -one type, platelets are small things. I imagine they're slightly squishy like a ball not quite taught with air but with the texture of a basket ball -the bumps representing lipids. In the living balls, the lipids constantly exchange, replacing each other. The enzyme responsible, phospholipase A2 (PLA2), may play a role in memory.PLA2 is not just in the tiny platelet cells; it's in a variety of other cell types including neurons. In the brains of victims with memory deficits, PLA2 activity is decreased. With the idea that the PLA2 activity in platelets reflects that of brain cells, researchers at the University of Sao Paulo in Brazil asked whether brain training exercises could increase the activity of this enzyme in healthy elderly subjects.The tasks researchers gave the subjects included a list recall exercise, much like the name task that I so dreaded. The experimental group was “trained” in four 90 minute sessions that included a discussion regarding memory and aging and a practice component that introduced the concept of mnemonic strategies (associating words with related meanings).Blood was taken at the outset of the experiment and when it was over two weeks later. Researchers tested for PLA2 activity... it changed, generally increasing with the exercise. One caveat: there are several types of the enzyme. Some of them stay in the cell, while others are secreted. One of them depends on calcium and another is calcium independent. This last one, calcium-independent PLA2, decreases in patients with Alzheimer's disease. This one, however, also decreased in healthy individuals that underwent the training.The paper concludes “the present data support the notion that cognitive training promotes biochemical changes that correlate with memory acquisition and retrieval... and illustrates the potential of non-pharmacological intervention to improve cognition in older adults through the modification of neurobiological systems.” So, learning can change your brain chemistry. And this change is likely paralleled in your blood.With the mentioned caveat, I wrote to Dr. Wagner Gattaz, lead investigator of the study. Here is his reply:I am also confused by this increment in iPLA2, I would expect exactly the contrary. I can not explain it. Therefore, the conclusion from our data is that cognitive training causes changes in membrane phospholiopid metabolism, in a very general manner.1. Cognitive activity through the life, as measured by years of school, reduce the risk for AD. This is one of the most consistent findings across several studies.2. PLA2 is low in AD3. Cognitive activity increased PLA24. Thus, this finding (3) may provide a biological rationale for (1)5. Maybe the use of cognitive training should be emphasized in individuals at risk for AD.We are now investigating the effects of cognitive training on PLA2 in patients with AD. Our question to be tested: does the enzyme activity also increase in these patients?After doing the naming exercise, I would love to have access to my own PLA2 levels and how they change over the course of the task, or better yet, a lifetime. Undertaking research on brain lipid biochemistry in people and trying to relate it to blood chemistry is quite the cognitive task. I wonder what Dr. Gattaz's PLA2 activity is.TALIB, L., YASSUDA, M., ODINIZ, B., FORLENZA, O., GATTAZ, W. (2008). Cognitive training increases platelet PLA2 activity in healthy elderly subjects. Prostaglandins, Leukotrienes and Essential Fatty Acids DOI: 10.1016/j.plefa.2008.03.002... Read more »
L TALIB, M YASSUDA, B ODINIZ, O FORLENZA, & W GATTAZ. (2008) Cognitive training increases platelet PLA2 activity in healthy elderly subjects. Prostaglandins, Leukotrienes and Essential Fatty Acids. DOI: 10.1016/j.plefa.2008.03.002
- May 14, 2008
- 07:28 PM
- 654 views
Spicing Up Mouse Muscles: Potential Therapy for Muscular Dystrophy
by Lisa Conti in Stimulating Aliquot
Preparing meat with turmeric occurs in kitchens daily but using spices to treat muscle disease is not a common occurrence. New research from Nanjing University in China shows curcumin, the compound in turmeric responsible for its yellow hue, alleviates a mouse version of muscular dystrophy (mdx) when injected.Duchenne's muscular dystrophy is a muscle wasting disease that results in severe disability and ultimately, death. What is striking about the article published in Molecules and Cells is that the pathology of the muscle fibers is largely prevented.In my research with potassium channels, I spent some time viewing plump dystrophic mouse muscles under the microscope. Normal muscle slices easily, folding onto the slide; cross sections show uniform fibers nicely packed with nuclei in the cell's corners. Muscles from mdx mice, conversely, fragment and shred during the cutting process. The muscle integrity is drastically compromised and that's noticeable even when you get a nice sample laying flat on the slide. Debris is packed between the misshapen fibers and the nuclei no longer associate with the edge of the cell but are now centralized.The figures in this study are impressive because the muscle fibers appear healthier and the mice regain strength. The mouse data looks similar to mdx mouse muscles treated with corticosteroids -the current standard therapy for people with the disease. These medications slow the disease but have significant negative side effects. Muscular dystrophy results from a deficiency in one protein, dystrophin. This protein, viewed as a pivotal component of a protein network, links a multitude of other proteins providing a physical framework for the cell. But what the study authors think curcumin is doing, has nothing to do with this protein assemblage.Curcumin is well known to interrupt another protein, NF-kappa B, involved with regulating inflammation and stress. The authors hypothesize that the damaging affects of excessive NF-kappa B activity is reduced by curcumin.Treating muscular dystrophy with curcumin is not a new idea. Another group, fed mice curcumin in hopes of lessening symptoms. But no effects were observed. The technique of injecting the compound seems to be the key probably because more curcumin reaches the blood stream and becomes available.Is injecting curcumin a possible treatment for human patients? Could it replace current steroid treatments -or be used with them to treat the disease even more effectively. The doses of curcumin discussed are likely nontoxic.Lead investigator of the study, Dr. Min-Sheng Zhu, Professor at Nanjing University in China, stated, “A daily injection is indeed difficult to be accepted for long-term therapy, but I think this difficulty will be overcome in the future if curcumin is effective in human as we expect. Actually, we have been making efforts to solve this problem. We don’t know whether curcumin can be used with corticosteroid treatment. Considering the side-effects, I think it should be OK.”But what do practicing clinicians think about this savory idea of spicing up muscles? I attempted to find out by sending email to a reputable muscular dystrophy specialist. Unfortunately, I did not receive a response. So I'm calling on you, my reader to help out. If you work in the realm of clinical treatment, know someone that does or have personal experience on the topic, the readers here and I would love to learn more.The image above, taken from Figure 2 of Pan et al. shows normal mouse muscle (C57BL/10), control mdx mouse muscle, and mdx muscle treated with curcumin.Pan, Y., Chen, C., Shen, Y., Zhu, CH., Wang, G., Wang, XC., Chen, HQ., Zhu, MS. (2008). Curcumin Alleviates Dystrophic Muscle Pathology in mdx Mice. Molecules and Cells, 25(4)... Read more »
Y Pan, C Chen, Y Shen, CH Zhu, G Wang, XC Wang, HQ Chen, & MS Zhu. (2008) Curcumin Alleviates Dystrophic Muscle Pathology in mdx Mice. Molecules and Cells, 25(4). info:PMID/18460899
- May 7, 2008
- 01:24 AM
- 631 views
Beer Goggles and Strobing Lights: What Your Brain Thinks About Alcohol
by Lisa Conti in Stimulating Aliquot
Neuroscientists have discovered -from the brain's perspective- what social drinkers already know: alcohol feels good, is relaxing, and you know how tipsy you are.Imaging activity in the brain while administering alcohol intravenously, researchers from Brown University and the National Institute on Alcohol Abuse and Alcoholism, investigated how alcohol relates to emotion. Subjects underwent functional magnetic resonance imaging (fMRI) while receiving alcohol or saline. During the procedure, they were shown pictures of neutral or threatening faces -a technique known to elicit a fear response.As expected, subjects given saline showed activity in the brain corresponding to regions relating to fear (including the amygdala) when viewing the threatening photos. The alcohol recipients, however, did not display this response. And, under the neutral image condition, they showed increased activity in areas of the brain having to do with pleasure and reward (ventral striatum).A striking proportion of the reward regions showed activity in the alcohol condition. That the brain is saying “cheers, this drink feels good,” has implications to the study of alcohol in relation to addiction and alcoholism treatment.The fact that alcohol abolished the fear response, readily triggered in control subjects, is intriguing. The authors speculate that because alcohol also affected the visual and limbic brain areas, an inebriated individual might see or interpret faces differently than their sober counterparts do. Perhaps this could explain the beer goggle phenomenon. Additionally, the data relating to the amygdala itself suggests it may play a role in misconstruing the presented expressions resulting in difficulty discerning friend from foe.An unexpected finding relates to how individuals perceive the extent of their inebriation. Perception of one's intoxication did not reflect blood alcohol levels. However, people could seemingly sense how active their ventral striatum was. The more activity in the reward center -swayed by circumstance- the more a subject reported drunkenness. So, while you might not be able to tell what your blood alcohol level is, you can tell how tipsy you are. Perhaps this could explain why the strobing lights of a night club are part of the party while the flashing lights of a patrol car are sobering.The above image, taken from Gilman et al. (Fig. 1A), shows activity in the ventral striatum in the alcohol condition.Gilman, J.M., Ramchandani, V.A., Davis, M.B., Bjork, J.M., Hommer, D.W. (2008). Why We Like to Drink: A Functional Magnetic Resonance Imaging Study of the Rewarding and Anxiolytic Effects of Alcohol. Journal of Neuroscience, 28(18), 4583-4591. DOI: 10.1523/JNEUROSCI.0086-08.2008... Read more »
J Gilman, V A Ramchandani, M B Davis, J M Bjork, & D W Hommer. (2008) Why We Like to Drink: A Functional Magnetic Resonance Imaging Study of the Rewarding and Anxiolytic Effects of Alcohol. Journal of Neuroscience, 28(18), 4583-4591. DOI: 10.1523/JNEUROSCI.0086-08.2008
- April 28, 2008
- 09:31 PM
- 613 views
Worming Your Way to the End –Smart Drugs For Schizophrenia
by Lisa Conti in Stimulating Aliquot
In 2006, a drug promising cognitive enhancement to people with schizophrenia emerged from phase I clinical trials. Press releases, message boards, scientific meetings, and blog postings rang out.This month, the schizophrenia phase II clinical trial results were released (Am J Psychiatry, Freedman et al.). As far as I can tell, no editorials or reviews accompany the paper. No press releases or message boards were updated. Even the blogger world has been silent. Albeit, I'm talking about a paper that came out ahead of print but that was a month ago. Here I will render its data into a story with a beginning, a middle; the ending –you decide.This is a provocative tale starting twenty years ago when a young researcher combed the rocky shores of Washington for small worms (Nemerteans). Dr. William Kem, now a professor of pharmacology at the University of Florida, still investigates invertebrate compounds for research as well as practical purposes.Dark on top with light bellies, these worms carry toxins that bind human brain receptors. I have yet to see one of these worms in the wild (despite hours of logged beach time). I was, however, fortunate enough to see a few faded versions floating in jars at Santa Barbara's Natural History Museum.In 2007, thirty one patients with schizophrenia were deemed eligible for the trial. DMXB-A (or GTS-21), the cognitive enhancing drug, would be administered alongside the patients' standard medications, the idea being that schizophrenia has multiple symptoms (only one of which is cognitive challenges) and may need to be treated accordingly. In addition, the subjects had to be free of nicotine or tobacco for at least a month.“You'd be hard pressed to find a schizophrenic that didn't smoke,” were the words that brought my attention to the link between smoking and schizophrenia. They came from a researcher at a Tobacco Related Disease conference who went on to explain that between 80%-95% of all patients with the disease use nicotine products. Smoking increases attention. Because people with schizophrenia have marked cognitive challenges, scientists attribute their nicotine use as a self-medicating attempt to focus.The problem with smoking (excluding the negative health consequences), is that receptors binding nicotine desensitize and effectively stop working. Increasing the dosage (the number of cigarettes, tobacco products -or even the patch/gum) works only temporarily and also results in significant negative physical reactions.Dr. Kem knew he had made a significant discovery when he realized the initial worm extractions had nicotine-like properties. For the clinical trials, DMXB-A was not purified from the worms themselves, but rather synthesized in a laboratory and placed into capsules.The original proof of concept study showed that when eight healthy Scottish men were dosed with DMXB-A, they performed better on tasks requiring focus and memory. In 2004, phase I subjects with schizophrenia were dosed and tested for just one day. The phase II tests were designed to determine effectiveness and safety in patients with schizophrenia for a longer term treatment -one month.Through the course of the month, some patients experienced trembling; some felt nauseated and restlessness. One patient became suicidal after a breakup with his girlfriend but the medication was not likely the cause. There were no significant adverse effects.But what about the cognitive effects? Did the patients get smarter?For me reading this clinical trial paper, it's really hard to tell. The answer seems to depend on the way cognition is evaluated. One analysis shows no improvement but the next offers promise. The patients report positively but placebo clearly betters things too. One sentence from the conclusion reads, “the clinical utility of this treatment is not yet determined.”The company currently investigating this medication, CoMentis, has also studied the drug in relation to Alzheimer's disease as well as attention deficit and hyperactivity disorder. I can tell you even less about those trials -except they have been completed.While the CoMentis scientific officer and Dr. William Kem were more than happy to talk with me -and very helpful regarding the drugs history and mechanism, they both referred me to Dr. Robert Freedman when my questions skirted to current study results. Unfortunately, Dr. Freedman declined an interview.This is where you decide the ending to this tale. Are the people involved quietly trying to lay this once thought giant to rest? Or perhaps this is the time before the big reveal? Or is it like many scientific stories -the ones not often told- where results are not black and white and data is a gray smudge worming its way from one side of a line to the other?For more information see Smoking Away Schizophrenia, a Scientific American Mind Head Lines article that I wrote.Kitagawa, H., Takenouchi, T., Azuma, R., Wesnes, K.A., Kramer, W.G., Clody, D.E., Burnett, A.L. (2003). Safety, Pharmacokinetics, and Effects on Cognitive Function of Multiple Doses of GTS-21 in Healthy, Male Volunteers. Neuropsychopharmacology, 28(3), 542-551. DOI: 10.1038/sj.npp.1300028Olincy, A., et, al. (2006). Proof-of-concept trial of an alpha7 nicotinic agonist in schizophrenia. Archives of General Psychiatry, 63(6), 630-638.Freedman, R., Olincy, A., Buchanan, R.W., Harris, J.G., Gold, J.M., Johnson, L., Allensworth, D., Guzman-Bonilla, A., Clement, B., Ball, M., Kutnick, J., Pender, V., Martin, L.F., Stevens, K.E., Wagner, B.D., Zerbe, G.O., Soti, F., Kem, W.R. (2008). Initial Phase 2 Trial of a Nicotinic Agonist in Schizophrenia. American Journal of Psychiatry DOI: 10.1176/appi.ajp.2008.07071135... Read more »
R Freedman, A Olincy, R Buchanan, J Harris, J Gold, L Johnson, D Allensworth, A Guzman-Bonilla, B Clement, MP Ball.... (2008) Initial Phase 2 Trial of a Nicotinic Agonist in Schizophrenia. American Journal of Psychiatry. DOI: 10.1176/appi.ajp.2008.07071135
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