The Collective

In the movie, Slither, alien zombies that look like giant pink slugs infect humans by wiggling through victim's open mouths.

I know this sounds like it has nothing to do with “real” neuroscience but bear with me here, I've been on a zombie kick.

The slug's first line of attack is through the brain, where necessary information relating to their species is disseminated, collectively linking all infectees. The zombie collective, consequently, know their celestial history, act in unison and are in love with the same woman.

After reading about mirror neurons, I can't help but reflect on how similar we are to the Slither zombies. Not that we all love the same woman, but we are, somehow, ethereally linked.

Mirror neuron cells activate when an observer sees an action or performs it. Researchers have recently shown that even observed facial expressions and hand gestures activate this mirror neuron system in humans. So, watching someones face (or hands) move, in turn activates the same brain areas that would fire if you were to make the movements yourself.

This system is likely responsible for the rubber hand illusion (how your brain can assume possession of a fake arm) that I spoke about last posting. How mirror neurons connect us with others or synthetic others (in the case of plastic arms), is likely the basis for imitation and empathy (and may have something to do with autism). And while it is characterized by action-linked responsiveness, some suggest that it may encompass or carry over into other realms such as emotion, or taste.

The cell biologist/biochemist in me wants to dissect these special cells and look at them on the single cell level. Are they at all different than cells that are not in the “mirror neuron system?” I imagine they are the same—but the activating stimuli is an idea, rather than a sensory perception. We all know that ideas can be infectious, stimulating and somehow amorphous. Perhaps the infectious nature of ideas and our brain's response to them is what makes us part of the collective.

In the zombie comedy, “Shaun of the Dead,” 'normal' people are so zombie-like, the main characters almost miss the uprising. Perhaps if we look long enough, we'll be able to dissect out all of our zombie tendencies. Until then, watch out for giant pink slugs.


There are lots of references for the mirror neuron system--this one is publicly available
Social cognitive and affective neuroscience 2007 Mar;2(1):62-66.

Halloween and the Rubber Hand Illusion

If you sit at a table with one arm on the table's surface and the other on your knee, then place a rubber arm on the table, positioning it as though it was yours, you can trick yourself into thinking the fake hand is your own. To do this, have a friend rub the rubber hand while they also rub the one balanced on your knee (using a similar stroke pattern). After a short time, you will feel as though the artificial hand is your own.

Several research papers have recently emerged regarding the rubber hand illusion. With an abundance of artificial arms (bestowed by stores tending to our holiday consumer inclinations), I couldn't pass up a zany opportunity: testing the rubber arm illusion on my friends and family. I purchased a plastic hand possessing surprisingly realistic pores, lines and even fingerprints. Given the ghoulish nature of the occasion, the arm also had a blood covered appearance. Here are some comments I heard while subjecting the good sports to the experiment:

“It doesn't feel like rubber.”

“It's like my hand moved up.”

“Mommy, can we stop now.”

“Huh, that's weird.”

As the brain combines visual and tactile experience it lets us know where our body is. For the majority of people, 15 seconds of synchronous sensation/observation—real and rubber hand together, results in the bizzare feeling that the hand on your knee moves to the surface of the table. In this state, the brain assumes possession of the artificial hand. And when scientists threaten to stab the “incorporated” fake hand with a needle, areas of the brain involved with anxiety and pain anticipation flare. Subjects report the worry levels synonymous with what they felt when the white coats came at their own hand with a sharp object. Similar experiments with no arm, but a virtual reality computer graphic, show subjects wincing with anticipation.

I can only imagine that these results are relevant to fields that include: 1) prosthetics (if I lost a limb, I'd surely want my doctors to know how to keep my brain from losing it—the limb that is), 2) psychotherapy (perhaps someone with the tendency to obsessively hand wash can come to grips with soiled hands if they utilize a therapy program involving a virtual system), 3) the video game industry (whether you're talking about how to get grandmothers to embrace Nintendo's Wii, or what the effects of video game violence are)—programmers, marketers and academicians, take note.

Now that Halloween is over, the arm resides in a box with cobwebs, spiders and a skull. Maybe next year, I'll tell you how to assume that glowing plastic cranium--the phenomenon after all, is not restricted to hands.

The Last Pop Stop: Popcorn, FAT and the brain

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, my husband 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, 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. The discovery suggests fat has its own flavor.

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.

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 oil
2 Tablespoons butter
Heat in a stainless steal popper with a turn paddle. Add
1/3 cup popcorn

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

MRI for the Fruit Fly

There were three bananas in the fruit basket before I left the house and when I got home there were none. “Where are the bananas,” I asked my husband. “He's a menace,” he replied motioning to the boy child. “I don't know, he was running around with them.”

I found one in my backpack that night. Four days later, I found one outside. The last one may have been eaten and at least some of the peels made it to the trash. But I did see two fruit flies on the bathroom wall. They are much smaller than house flies, not as annoying, and... not as fast. I didn't take much time to contemplate the value of the species to science and medicine before I squashed them.

The fruit fly, Drosophila, has been an incredible tool for scientists. They're cheap, fast growing, easy to mutate, and their genes are surprisingly similar to humans. Laboratories all over the nation and world are churning out lots of data on the bugs.

A new study headed by Ronald Davis at Stanford University, introduces a technique that might make future fly data even more... fruitful. Using a Magnetic Resonance Imaging (MRI) technology, the researchers imaged several life stages of Drosophila. What makes this different from standard microscopy is the organisms can stay alive.

When I first saw the report, I imaged the machine that I've seen at the hospital. A large tubular thing with a white padded table--in the middle sitting a tiny fly. The device used in the study, however, looks more like something you'd brew beer in.

The prospect of imaging the live organisms with time has far reaching implications for studies relating to many fields including development and neuroscience. In fact, the ability to “see” neurotransmitters and use complementary techniques involving genomics are intriguing avenues discussed by the authors.

Now, if only I could image my house and find the remains of our own Drosophila breeding experiment.


Null, B., Liu, C.W., Hedehus, M., Conolly, S., Davis, R.W., Zwaka, T. (2008). High-Resolution, In Vivo Magnetic Resonance Imaging of Drosophila at 18.8 Tesla. PLoS ONE, 3(7), e2817. DOI: 10.1371/journal.pone.0002817

Hand in Hand

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

Filtered Science

I ask every science writer I meet the same question.

Trace science blog articles back to the primary literature and you'll notice a strikingly high proportion source from open access articles. This goes for many news headlines too. Especially freelance science writers are disabled when it comes to accessing journal articles.

When I was a university employee, it was easy to take the library -the access- for granted. The process by which scientists and their discoveries make headlines or blog lines didn't seem a mystery when I had gloved hands. Fascinating science was obvious. The experiments leaped out of the journal. Even if the science wasn't ground breaking, the topics were gripping and the experiments, telling.

But now that my gloves are off and my password not functional, titles jump from the screen, topics may seem tantalizing -but they're just titles, topics and abstracts. Getting the article, the details of the research -or the background- is another story.

My question to the science writers I meet: Access, how do you get it? The solutions I've come across are always disappointing. The best involve relying on open access articles and retrieving the articles directly from the author. Sure there are ways; but the once deft, gloved hands are now somewhat tied.

What's more disappointing than not having fingertip access to all the cutting edge research, is the realization that the public in turn doesn't either -the science to some degree is filtered.

Sea Lions Suffer

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

Rotten Eggs

The other day I discovered our chicken's hidden nest with under the oak tree in the front yard. As someone with little chicken experience, I was inclined to immediately toss all twelve of them. The newest addition had to be at least a week old. For reasons I still don't understand, I was a bit squeamish about the whole thing. Determining that the feelings were irrational, I sent my four year old daughter to collect the eggs and called my husband for consult. My optimist husband, practical regarding such matters, gave me a quick biology lesson, “The bad ones will float.”

They float because with time, they dry leaving an air bubble. In our case, two of the eggs sunk down to the bottom of the bowl, eight stood on their end and two bobbed to the top. The optimist assured me that the eight eggs may not be bad, “You have to smell them.”

While I've never smelled an actual rotten egg, I know it's bad. And I wasn't about to risk nausea or illness to test the limits of my sensitive detection system. I'd had enough of the experiment and gave the girl child permission to throw the bowl of ten into the compost pile.

All the while, a mental image of one sulfur and two hydrogen atoms was bobbing around in my head. Hydrogen sulfide is a bacterial byproduct -a gas. I thought about what receptors the small molecule bind to and as always I like to reflect about its affect in the brain.

Too much of the gas is poisonous. It passes through cell membranes and shuts down cellular metabolism -in the lungs and in the brain. The toxicity reported is comparable to cyanide.

But hydrogen sulfide is also produced in our own tissues (independent of bacterial infection) as a part of our normal biology. The gas, termed gasotransmitter, is a neurotransmitter and represents a whole subfield of neuroscience. It is involved in maintaining the tone of blood vessels, the transmission of signals between brain cells and even insulin secretion.

Ironically, the primary characterized target of the gas is the molecule that I wrote my dissertation on, a potassium channel expressed in the brain, heart, and blood vessels.

My daughter hesitates before tossing the eggs “why can't we eat them?” she asks. “Because they might be stinky,” I answer saving the lecture on the potential role that hydrogen sulfide plays on the macromolecules in her brain.

Related reviews:
Leffer et al. 2006
Wang 2002

Your Memory Is In Your Blood

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 AD
3. Cognitive activity increased PLA2
4. 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

Spicing Up Mouse Muscles: Potential Therapy for Muscular Dystrophy

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)

Hormone Junkie: Treatment for Multiple Sclerosis

The MS solution, a book written by Kathryn R. Simpson, tells the gripping story about the author's own experience with multiple sclerosis (MS) and how she renders herself symptom free. Using hers and other case studies she illustrates the point: replacing hormones treats the disease. Written for people with MS, it guides the patient through the medical realm of neuroendocrinology.

I have read about studies -clinical trials even- that use estrogen or testosterone to treat multiple sclerosis and only wonder, why, if it works so well, it's not used more. Why aren't neurologists pouncing on this technique? She writes to this in the final words:

I will be the first to admit that this is a cutting-edge medical approach to MS; there aren't many doctors who specialize in treating hormone deficiencies, let alone have experience with using them in treating MS. You may be lucky and have an open-minded neurologist who will work with you on testing your endocrine system to see if this is a potential solution for your symptoms, but truthfully, I have found that this may not be the best medical specialty to work with in this approach. It's so far removed from a neurologist's medical training and clinical practice that it may be easier to find a forward-looking general practitioner or endocrinologist who has some exposure to hormone testing and treatment.

Simpson relates the disease to hormone equilibrium discussing the roles of estrogen, testosterone, thyroid hormones and others. Through her story, she touches on each and every hormone, how they decline with age, and how this relates to disease. By carefully replacing her hormones (lots of them -maybe, most of them), she describes how her symptoms vanish.

The book is inspiring and easy to navigate, while based in real science and believable anecdote. My only criticism is the cutting-edge research is cut a little short. Clinical studies were left without mention. This does not at all diminish the potential the “solution”. In fact, should I develop the devastating symptoms that accompany such a neurological disease, I'd soon be a hormone junkie.

Beer Goggles and Strobing Lights: What Your Brain Thinks About Alcohol

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

Worming Your Way to the End –Smart Drugs For Schizophrenia

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.1300028

Olincy, 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

Honey Dressing Wound Care Part II

In a correspondence with Professor John E. Moore of Northern Ireland's Public Health Laboratory regarding his MRSA/honey publication, he mentioned two important factors to consider when using honey for wound dressings:

Patients should use only medical-grade and not honey plucked off the shelf in their nearest food store. This is not a tactic to boost Big Pharma profits, but a very necessary step to avoid potential infection from dormant bacteria in foodgrade honey. Such honey is not sterile but may contain many spore-forming organisms, which is not a good idea to apply to a wound. The medical grade honey is sterilized to wipe out such bacterial contaminants.

Infant botulism: One spore-forming contaminant may be Clostridium botulinum. Therefore newborns and young children should avoid ingesting natural honey to avoid getting infant botulism. There may be a temptation for young children to “taste the cure”.

Cheers to Professor Moore for bringing this fascinating topic to us -see previous post for full story.

Honey Dressing: Treating Methicillin-Resistant Staphylococcus aureus

The threat of hospital and community associated Methicillin-Resistant Staphylococcus aureus (MRSA) has clinicians, parents, and the infirmed panicky. New research, not to mention ancient practices, suggest that a medication-free solution may be sitting in our cupboards.

Two weeks ago, I watched my two year old son play in a mound of worms and rolly pollies located in our back yard dirt pile. Had I known that within his blue sandal a small cut on his fourth toe was beginning to fester, I would have washed more than his hands upon entering the house for a snack--on this occasion yogurt with honey.

Staphylococcus aureus, named for the golden color of its colonies (aereus was an ancient Roman gold coin), is a spherical bacteria that forms clusters. Found on skin, in noses, and in dirt piles, it's unavoidable. The intensity of the yellow pigment is proportional to the severity of infection. While the pigment doesn't cause drug resistance, there is an association with virulence and infection intensity. MRSA is scary not just because it is resistant to treatment with antibiotics, but also because it is extremely aggressive.

When our pediatrician saw the toe four hours after prescribing an oral antibiotic, she took a step back. The speed at which the infection was progressing made her suspect that his growing purple blister was concealing a MRSA bug. He was hospitalized immediately and placed on intravenous antibiotics.

For me the idea of squirting honey on an open wound is akin to bandaging a chocolate bar to it. But well before the advent of antibiotics ancient peoples used it regularly. It is also currently utilized for similar treatments in parts of the world outside of the US. When I first heard this, I imagined places ill equipped with medical supplies--places where drinking water, let alone intravenous antibiotics, is scant. This is not the case. Experts in New Zealand, Germany, Ireland and other places are dipping gauze in the amber gooiness and pushing it against the nastiest injuries.

The scientific reports are astonishing. Researchers growing bacteria on petri dishes watch colonies disappear with honey application. Doctors have seen children once needing anesthesia for a dressing change, hardly wince with application. In addition to anecdotal data, one randomized control trial concluded “There was no evidence of a real difference between honey and IntraSite Gel as healing agents. Honey is a safe, satisfying and effective healing agent.” Studies comparing other agents with honey on the treatment of ulcers report greater healing power of honey dressings.

Historical studies determined the effectiveness results from honey's osmotic properties. The bacteria, having more water in them than the honey, literally shrivel and die. This attribute, however, is contradicted by the diluting effect of a weeping wound. Never-the-less, experiments repeatedly show the therapeutic effectiveness in the treatment of Staphylococcus infected wounds. Honey also has enzymes with antiseptic bi-products (namely, hydrogen peroxide). While scientists continue to unravel the reasons for its potency, data is showing that it works even for bacteria harboring antibiotic resistant genes, MRSA!

Despite antibiotics, the blister was growing fast and had an ominous appearance. With a team of six clinicians (including two pediatric surgeons), blue gloves gripped scalpel and forceps, hovering bright lights were centered, nurse readied with gauze dripping brown liquid, and doctor pushed anesthesia through an intravenous tube. As the scalpel poked through the skin, cloudy fluid spurted past the table and onto the floor. Swabs, rubbed on the inner surface of the skin, were placed in test tubes and sent to the laboratory. Freed from the infected skin, the remaining wound was wiped, coated with a white creamy topical antibiotic and wrapped with gauze. We were treated similarly and transferred to an isolation room. Entering staff had to suit up in blue plastic aprons and gloves, meal trays were left outside the room and visitation was discouraged. It seemed that the only thing entering the room were clear bags of antibiotics.

While there are claims that honey from particular locations carry more antiseptic properties than others (including anti-fungal and anti-viral properties), with some even marketed as medical grade honey, the fact that all varieties tested demonstrate antibacterial properties should be enough to transfer the kitchen product into our first aid kits. So why is it that today after meeting with our pediatrician, I filled the prescription for a topical antibiotic and dutifully dressed the still healing wound?

Honey is healing and cost-effective but until clinicians embrace it, it's useless. Our culture confides in the advice of white coats handing out prescriptions. In order for the golden liquid to effectively combat the golden colonies, we need to embrace ancient wisdom and current research at the level of the doctor's office.

Incidentally, the bacterial culture results revealed the toe culprit to be a simple everyday Staphylococcus aureus, not the dreaded MRSA.

***
Also see Professor Moore's comments regarding this post and medical grade honey.

Some of many relevant references:

Yapucu Güneş U, Eşer I. Effectiveness of a honey dressing for healing pressure ulcers.
J Wound Ostomy Continence Nurs. 2007 Mar-Apr;34(2):184-90

Ingle R, Levin J, Polinder K. Wound healing with honey--a randomised controlled trial. S Afr Med J. 2006 Sep;96(9):831-5.

Boukraâ L, Niar A, Benbarek H, Benhanifia M. Additive Action of Royal Jelly and Honey Against Staphylococcus aureus. J Med Food. 2008 Mar;11(1):190-2.

Maeda Y, Loughrey A, Earle JA, Millar BC, Rao JR, Kearns A, McConville O, Goldsmith CE, Rooney PJ, Dooley JS, Lowery CJ, Snelling WJ, McMahon A, McDowell D, Moore JE. Antibacterial activity of honey against community-associated methicillin-resistant Staphylococcus aureus (CA-MRSA). Complement Ther Clin Pract. 2008 May;14(2):77-82.

Sweet Pleasure: Calories Register Reward Independent of Taste

That the brain has the ability to appreciate calories hedonistically without input from the tongue is a momentous report. A new study, using mice incapable of tasting sweetness, determined that the brain's pleasure system is activated when sugar is consumed independent of taste.

When the mice consumed sugar -whether they could taste it or not- dopamine levels increased suggesting that the mice were experiencing pleasure. When given a choice, taste deficient mice like normal mice selected the sipper containing a sugar solution over water. But when artificial sweetener was substituted, the “sweet blind” mice showed no bottle preference or change in dopamine levels indicating that the feel good effect was due to the calories.

Interestingly, mice with intact sweet taste did not have a greater pleasure effect from sugar than the artificial sweetener. So does taste trump calories? The authors imply that it might not and speculate that obesity and overeating may involve this calorie sensing sweet pleasure.

. de Araujo IE, Oliveira-Maia AJ, Sotnikova TD, Gainetdinov RR, Caron MG, Nicolelis MA, Simon SA. Food reward in the absence of taste receptor signaling.
Neuron. 2008 Mar 27;57(6):930-41

Do You Need Another Reason to Drink Coffee?

A new study suggests that you can have your cake and eat it too -or at least, have your caffeine and protect your brain from damaging dietary cholesterol.

The report shows that caffeine counters the negative influences that high cholesterol can have on the brain without changing the blood cholesterol levels. Giving rabbits a high cholesterol diet in addition to caffeine (equivalent to one cup of coffee a day), researchers at the University of North Dakota tested the hypothesis that “chronic ingestion of caffeine protects against high cholesterol diet-induced disruptions of the blood brain barrier” in their recent Journal of Neuroinflammation publication.

Previous studies indicate that caffeine protects the brain from neurological diseases such as Alzheimer's disease. What makes this study interesting is that it provides a mechanism for the protective effects. High dietary cholesterol compromises the blood brain barrier (a network of cells that line small blood vessels to impede damaging compounds circulating in the blood stream).

The authors point out that the finding has two therapeutic implications. One being that caffeine consumption may be used as a treatment for brain diseases by itself. The other is that withholding caffeine might facilitate the entry of other medications into the brain.

So what is caffeine doing to prevent cholesterol induced breakdown of the blood brain barrier? It blocks reduction of specialized proteins that join cells together. In other words, caffeine sustains the proteins that physically bind one cell to the next.

Another interesting caveat is that increasing the caffeine dosage (by ten) did not change the effect. However, to achieve protection the dosage did need to be “chronic”. So take comfort when having your daily cup of coffee.

The image above (from Fig 1 of the sited paper) shows that when caffeine is present, cholesterol-induced blood brain barrier damage is prevented. The brown splotches are areas reactive to blood factors that seep into the brain following leakage.

Xuesong Chen, Jeremy W. Gawryluk, John F. Wagener, Othman Ghribi and Jonathan D. Geiger, Caffeine blocks disruption of blood brain barrier in a rabbit model of Alzheimer's disease, Journal of Neuroinflammation 2008, 5:12 doi:10.1186/1742-2094-5-12

Fishy Brain Cells Take Sides

One of our fish has an unnaturally long fin on its left side. I call him Flag Fin. Our tank houses ten zebrafish: small, cheap and hearty. Our fish were intended for conditioning the tank -to prepare the environment for more sophisticated creatures- but we never got around to flushing and replacing them so here they are, swimming.

Most things have direction in life -with reference sidedness, not purpose. The snail collective dutifully scrapping algae off the tank's walls all have shells that spiral to the right (though I understand the shells can coil counterclockwise). To notice this lopsidedness in yourself, look at the reflection of your reflection. It really brings out facial asymmetries.

Most days, I walk by the tank without taking notice. But today, I sit next to it and look closely. One fish has a bulging belly. One looks almost orange between the dark stripes. And then there's Flag Fin. All of them have equally small heads. Tiny, pea-sized heads.

That brains have sides is no news. How our right hand corresponds to our left brain, or how our verbal skills are distinct from our musical talents, has scientists linking regions with function left and right.

Only recently did I make the connection that the zebrafish used in lab experiments are the same feeder fish swimming in my living room. A study published last week in Neural Development used the fish to show that the brain's asymmetry coincides at the level of single neurons.

Two pea sized nodes in the human brain (the habenula) have been implicated in functions including control of the circadian rhythm, behavior and mood. In the zebrafish, this structure is notably lopsided.

The researchers based at University College London embedded the fish embryos (no longer than the width of a toothpick) in a gelatinous substance and injected DNA corresponding to a green or red fluorescent protein using a series of electric pulses. This enabled them to visualize individual brain cells that display elaborate shapes. What they saw was telling. Looking at cells from the left and right habenula, the team noticed an unprecedented feature. The axons crossed over to the other side -not once, not twice, but lots of times. In fact, they made spirals.

The team also noticed that most of the cells on the left looked different than those on the right. The shape typical of left cells were “domed crowns” and the right-typical looked more flattened and shallow.

This experiment exemplifies reductionism on two levels: 1. the brains microscopic building blocks dictate or “encode” the macroscopic shape and 2. primitive critters are important to advanced concepts.

Zebrafish have primed so much more than a fish tank for the introduction of more sophisticated content. How our brain cell morphologies dictate asymmetry and how that corresponds to differences in behavior and cognition will keep scientists whirling in experiments.

Inside the glowing tank, Flag Fin waves. I imagine a spiraling green cell deep in his little brain. “Good night Flag Fin,” I say, flipping off the light.


The images displayed above show cells from the larval zebrafish habenula that extend into spirals. They correspond to Figures 1C and 2A from the article referenced.

Isaac H Bianco et al. 2008

Nutty Brain Humor

Every year on April first, I play a small prank on my husband. The jokes are not incredibly funny but we (well, I) manage to get a chuckle. Since I have a hard time keeping a straight face, I usually set up an ambush -think, bath towel laced with glitter dust.

What makes silly jokes funny?

One year when I was a grad student frantically pulling together a journal club presentation, I came across reference to a brain region called the amygdala. In consult with a professor, I asked about the brain area. He was either unaware or had a good sense of humor; his response was “I don't know, a dance?”

Data from functional magnetic resonance imaging suggests that the amygdala (particularly the structure on the left side of the brain) is involved with the emotions relating to amusement. But the amygdalae are funny things linked to critical functions including fear conditioning and maternal behaviors.

While the general role of the amygdala in associating memories with emotional events explains the smile I get when seeing glitter remnants in the caulking, I'm sure that the science of humor is more convoluted than activity in one nut sized region.

Bartolo et al. 2006

Yellow Spice Brightens Wit?

I love a good curry. But what I really love is a good curry that provides brain power. A study published in the March 24th JBC Papers in Press suggests that curcumin (a component found in the spice turmeric) stimulates the generation of brain cells.

What is interesting about this study is not just that curcumin is an antioxidant or protective to neurons in culture (cells grown in petri dishes) but that low doses promote the generation of new brain cells in living mice. What makes the study even more enticing is that the cells sprouted in the hippocampus of adult mice.

As we're all too aware, the older we get, the less eager our brain is to develop cells. The hippocampus, a region devoted to learning and memory, is compromised by age and ravaged by Alzheimer's disease. The study authors speculate that curcumin stimulates synaptic plasticity (increasing connections between brain cells) in the same way that exercising does.

There is some discussion regarding the dosage -as too much may negate a desired effect. But the possibility that a portion of good curry might brighten more than just a bowl full of rice puts the dish on my menu.

The above image, from the original PDF, shows the hippocampus stained with a reagent that detects proliferating cells. As you can see the Cur (mice treated with curcumin) have more proliferating cells than control mice, Con (treated with saline)

Kim et al. 2008

Falling without Falling

My son's tendency to run full throttle, regardless of height or hazard, has given me opportunity to experience two new physical phenomena. Every time I see him stumble, I experience a falling sensation. Not a little yikes but a full blown stomach plunging I'm dropping feeling. Second is my surprising ability to catch him.

After reading The Body Has a Mind of Its Own by Sandra Blakeslee and Matthew Blakeslee (a captivating read), I have a renewed appreciation for how the brain and body network together.

Areas in the brain are devoted to keeping track of limbs, body parts, and other items within close proximity to the body. Moreover, these areas are malleable. With months of carrying and holding my son, my brain's ability to assimilate his form into my own body map may be what's going on. This gives the term "attachment parenting" a whole new physical meaning. Could my brain view my son as an extension of my peripersonal space (the space around the body) even when I'm not holding him? Could this explain why my innards drop as I witness him trip?

And what about my new found agility. I caught him by the ankle as he dove, smiling, head first off the jungle gym at the park. I grabbed him mid air, under the arms as he leaped off a picnic table in cannon ball formation. And I ever so fluidly prevented him from a face first impact when he bounced off the top bunk bed. I couldn't have performed those tasks if I put my mind to it. Maybe his gleeful inability to grasp consequence is really a profound understanding of my reaction limits. Perhaps his brain has incorporated me as an annex map, so-to-speak, of himself. After all, an ear to ear grin develops in concert with me stepping into catching range.

Dancing Eyelid

Well, it's happening again. My right eye just below the brow is twitching. In 2001 I had an eye twitch that lasted for three weeks! When you're constantly feeling your eye quiver, three weeks is a long time. I fear an eternal twitch.

As someone who spent years looking at muscle under the microscope, I can visualize the long slender striated cells glowing red with umpteen blue dots -many nuclei. Imagining calcium flowing through channels embedded like donuts in the cell's membrane, I think, Yes, I need potassium and reach for the bananas.

I first noticed it while brushing my teeth. Looking close, I saw it go. Like a small creature trying to get out, the muscle struggled. It twitched through breakfast. It twitched through the credit card transaction at the grocery store, and it moved to my rendition of Bo Diddly's Mona while I practiced the guitar.

Maybe it was caused by the piece of glitter that took two days to find and extract (an occupational hazard). Or maybe it's because of fatigue or stress (that's what my opthamologist would say). Or perhaps it's a sign of serious neurological doom (my brain just goes there sometimes).

Serious persistent eyelid spasms, blepharospasm, is associated with neurological conditions like Parkinson's disease. Sometimes damage to the basal ganglia (a structure of the brain responsible for motor control and many other things) causes the problem. But really, no one has been able to map out the mechanism behind this irritating phenomenon and I am relieved to find out that it's rare to identify a condition in which to link it.

And if it does go on and on there is a treatment -injection of botulinum toxin. Famous for treating wrinkles, the paralyzing poison promises that the eyelid will loose its groove.

Aminomen

I wrote Aminomen, a silly graphic biochemistry book, with kids in mind. It turns out that adults get a kick out of it too. It introduces concepts and terminology with a series of amino acid characters, each associated with a biochemical attribute. I'd like to think that it associates biochemistry with levity and simplicity. My daughter already knows that cysteine is responsible for her curly hair.

The Devastating Loss of Tongue Dexterity

With my recent toxic plant preoccupation, I have received an assortment of interesting anecdotes including one regarding the yellow star thistle.

Horses that forage on the tall spiny yellow flower die of starvation. Under the impression that the plant causes an obliteration of appetite, my interest was piqued -especially since my second current preoccupation is how the brain responds to food in the satiation/hedonistic sense.

The disease, following ingestion of this nasty invasive, is called equine nigrapallidal encephalomalacia (how much tongue dexterity do you need to say that?). While the cause of death is starvation (or dehydration), loss of appetite is not the reason. It turns out that the plant's toxins result in brain lesions in areas having nothing to do with detecting food volume, taste or calories; they have to do with fine motor control. For a horse, the only thing that requires intricate movement ability is the tongue.


Moret et al. 2005
Sander et al. 2001