Certiorari emptor; on informal routes of public science education

A recent editorial by Dr. Royce Murray, editor of the journal Analytical Chemistry, has garnered significant attention in its attacks on informal dissemination of scientific information to the general public. Given that public education of science is a relevant topic to this blog, I thought it merited a response here.

The basic premise is that the only trustworthy sources of scientific information that can be given to the general public are peer-reviewed journal articles and a small number of established news sources, the latter of which Dr. Murray correctly admits are faltering. To distill his point further, he doesn't like the rise of scientific blogging.

I readily agree that, "The picture of scientifically grounded innovations feeding progress in science is well established. I firmly believe that this system has served science well and that the scientific literature has provided generally reliable information and vast benefits to society over the centuries to the present and will continue doing so into the future." It's true that this information should reach the public for many reasons, including that it protects the public, reduces stigma and susceptibility to pseudoscience, influences public policy, and fosters a sense of scientific wonder in prospective scientists and non-scientists alike.

However, I reject the premise underlying his statement that, "...editors and reviewers reinforce the meaningfulness of Impact Factors by explicit attention to the reliability of submitted articles; if the Scientific Method has not been adequately followed, then there should be a downwardly adjusted evaluation of impact." This is a misrepresentation of impact factor, the measure of how frequently a journal's articles are cited relative to the number it publishes. Impact factor does not measure the extent to which an article follows the scientific method whatsoever; it is more an index of how novel and important, on average, an article published in a particular journal is likely to be, as assessed by how frequently other scientists refer to it in their own articles. The principles of impact factor, far from applying only to peer-reviewed sources, apply just as accurately to informal sources, in that their quality and novelty determine their audience and are reflected by how frequently they are referred to and discussed.

More importantly, it's false to say that the optimal venue for dissemination of knowledge from scientist to layperson is necessarily a published journal article. Scientific articles are not accessible to the general public, even to those members that actively seek them out; restrictive language and jargon, in tandem with prohibitively high costs for accessing articles, prevent access to anyone aside from university-affiliated experts in the respective fields, which defeats the entire concept of limiting the scientific information available to the public to peer-reviewed articles.

In agreement with Dr. Murray, I'm not a fan of the word 'blogger' or its derivatives, but I fear by his attempted definition that he does not understand the term, in that he assumes their primary motivation is to be "entrepreneurs who sell 'news'". This blatantly overlooks the fact that the vast majority of the population he attempts to describe act not out of personal financial gain but rather out of an altruistic desire to educate, and this is especially true of scientific writers in this medium.

Dr. Murray warns, 'caveat emptor'; let the buyer beware, as communication through informal channels increases the risk of malicious misinformation. I propose an alternate viewpoint. Certiorari emptor; let the consumer of these media be informed. This is the ultimate goal of those who seek to educate regardless of medium.

References:

Murray, R. 2010. Science Blogs and Caveat Emptor. Analytical Chemistry 82: 8755.

- Ian Mahar

(Adapted from an article originally appearing here).

Electricity and the brain

Part 1 of 3 : Ions

Most people know that the brain uses electricity to operate. However, what most people do not realize is that the electricity produced by the brain is different from the one produced by batteries or the companies that provide electricity to your home. Indeed, the source of electricity in these examples comes from chemical reactions or from natural resources. This electricity is then routed to your house, for your use, by transfer of electrons between metal atoms that make up the electrical wiring. We can thus define electricity as a movement of electric charges between a potential difference or voltage. However, the brain uses a slightly different system to generate and propagate electricity. Some basic concepts are needed before we can understand how brain cells (neurons) generate electricity in their cell body and propagate it along their axons (Figure 1).

Matter can be divided into basic elements called atoms. Calcium, sodium, potassium and chlorine are examples of atoms. Table salt contains mostly sodium chloride, that is a sodium (Na) and a chloride (Cl) atom. If the two atoms are to be held together, each atom carries a charge (sodium has a positive charge and chloride has a negative charge). Since each atom has an opposite charge, they attract each other, much like the poles of two magnets. However, the forces that attract these two atoms are weak so that when you put the salt in an aquarium filled with water (Figure 2), atoms dissociate to form ions, a positively charged sodium (Na +) and a negatively charged chloride (Cl-). The atoms then diffuse so as to be uniformly distributed in the aquarium. It must be noted that although the atoms of the salt are dissociated and they are charged, the aquarium is electrically neutral (as much positive charges as negative charges).

Adding other specific components in this tank (potassium chloride (K + and Cl-), magnesium chloride (Mg 2 + and 2Cl-), glucose (sugar), calcium chloride (2Cl- and Ca2 +), sodium bicarbonate (Na + and HOCOO-), proteins and oxygen) will result in a uniform distribution of these constituents in the aquarium. We then get a liquid that roughly reconstitutes the fluid that neurons bathe in (cerebral-spinal fluid).

Eric Trudel

Neuroscientific Art

Exactly where the threshold between Science and the Arts lies can be a touchy subject. Like a lot of dichotomies that were once assumed to be fixed opposites, these days it’s looking more like there is a science - arts continuum. This is particularly valid in the nebulous field of neuroscience, where the overarching goal is to bring together disciplines that study the mind and how it works - like philosophy, sociology, psychology - with fields that study the physical processes that underlie brain function - such as neurobiology, -chemistry and electrophysiology. A word to the wise: before you get into the science/arts debate with someone who studies the mind or brain, resign yourself to accepting them as a scientist - safer to keep your reservations about their place on the spectrum to yourself. (Personally, I think we should all call ourselves artists in keeping with the Latin use of “Art,” meaning skill or craft.)

While the debate rages over what should be included in the realm of “Science,” some scientists are working hard to go the other way. A number of Microscopic Art competitions have sprung up, showcasing beautiful images taken by biologists studying things too small for the human eye to see in all their glory. You may have seen the perennial scanning electron micrographs of pollen in National Geographic, but events like Olympus’ BioScapes and Nikon’s Small World Competition comprise images of many different subjects taken by many types of microscopes (the type of microscope used can drastically change the flavor of the picture). This year’s Olympus Bioscapes competition winners were announced last week, and neuroscientists took 1rst, 3rd and 7th places plus some honorable mentions. Take a look here.

The Incredible Human GPS

        Ever wonder how a cab driver is able to get you from point A to point “who knows where” without using GPS? Its cause his brain is bigger than yours… well… his hippocampus is. The hippocampus is a region in the brain important for long-term memory and spatial navigation. While it was long thought that talents were innate and had to be nurtured at a young age, researchers studying London cab drivers say that an old dog can learn new tricks. London cab drivers have to learn the layout of over 25, 000 streets through 3-4 years of schooling after which only 25% of aspiring cabbies make it out with a London cab certificate to attest to their ability to find their way through the city’s complexly interconnected web of streets. Through Magnetic Resonance Imaging, researchers have determined that London cab drivers have an increase in volume of the back part or posterior part of their hippocampus, indicating that the adult brain is still capable of changing its structure to meet certain demands. This means that talents are not necessarily innate but can also be acquired through repeated application. That’s right. Practice does make perfect.

        When compared to non-cab drivers or bus drivers, who follow a simple set route, cab drivers have a larger posterior hippocampus, which grows with years of cab driving experience, demonstrating that the posterior portion of the hippocampus is important for spatial representation of highly complex environments. However there is a catch. While the posterior portion of the hippocampus grows larger with driving experience, the anterior or frontal portion becomes smaller than those of bus drivers and non-cab drivers. This decrease in anterior hippocampal volume has been associated with a decrease in anterograde memory performance, that is, while cab drivers were better at spatial representation they were deficient in acquiring and retaining other new types of information such as directing movements in space as indicated by their lower performance in the Rey-Osterrieth test. This means that when cab drivers were shown a complex line figure and asked to draw it from memory, they were able to recall less than than bus drivers or non-cab drivers.

        Cab drivers don't only show that practice makes perfect, they also show that if you don't use it you lose it. Researchers compared the hippocampus of present cab drivers to retired cab drivers and found that the structural changes that occur in full-time taxi drivers are reversed in retired taxi drivers. Furthermore, retired taxi drivers scored less on their ability to navigate around London, however performed better in the Rey-Osterrieth test than full-time cab drivers.

        These observations are a testament to the fact that the adult human brain is not static but is quite dynamic, always adapting to our surrounding environment. This has implications in several fields such as education or rehabilitation of patients with cognitive impairments such as autism or even in Parkinson's disease. Researchers at UCL believe that with the right brain exercises we can strengthen those parts of the brain that are deficient or damaged. So those of you who claim to be "too old" to learn anything new, pick up that crossword puzzle, take that class you've been dying to take, start a new hobby and practice, practice, practice!

                         Michael Tibshirani

                          McGill University

Head and Shoulders, Knees and Toes...

Part 1:

If you found out that you were going to lose the use of your arms and legs in the next two years what would you do?

  ALS, more commonly known as Lou Gehrig’s disease, is one of the most common neurodegenerative diseases and is characterized by the death of motor neurons. Motor neurons are cells located in the brain and spinal cord that send out long projections and control your muscles, sort of like the electrical wires of the body. If these wires are removed, muscles in your body won’t get the message to move. This means that those diagnosed with ALS experience a progressive paralysis, losing the use of their bodies one part at a time. Every year 1 in 100,000 people are affected by ALS; slowly losing their independence, unable to walk, speak, or even express emotion through facial expression while still fully aware of their surroundings, trapped in a body that won’t listen to them.  Eventually, usually within 2-5 years of diagnosis, patients die from respiratory failure because the motor neurons controlling the muscles that help you breathe die as well.  This devastating disease can affect anyone. Although the usual onset of ALS is between 40-70 years of age a small proportion of ALS sufferers experienced symptoms, like the great Stephen Hawking, in their early twenties. It is twenty percent more common in men than in women however the incidence is more equal among men and women with increasing age. 

The cause of ALS is still a little unclear and is thought to be a multifactorial disease and so research has investigated several disciplines such as inflammation, excitotoxicity and cell-cell communication. While only 10% of ALS cases are familial, meaning the cause can be linked to defects in your genes, 90% of cases are sporadic, however there is a silver lining to this. When we look at nervous tissue taken from ALS patients, the common characteristic we find between both familial and sporadic cases is the presence of protein clusters called aggregates. By studying familial cases and the genes involved in ALS, we can generate models that allow us to investigate the mechanisms behind ALS and what makes motor neurons particularly vulnerable to protein aggregation. 

In normal cells, proteins initially come out as a string that must be folded properly to function. When these proteins are misfolded either under cell stress or as part of a disease pathway, they tend to stick to each other and form clumps or aggregates in the cell, which interfere with various cell processes and, if not taken care of, will lead to cell death. Whether protein aggregate formation is the beginning or the end of the pathogenic pathway involved in ALS, it is clear by experimentation that motor neurons don’t like having aggregates in them, and so a lot of ALS research has been focused on trying to understand the role aggregate formation plays in the pathogenesis of ALS.  In the next segment we will discuss current research, which explores the cell’s responses to these aggregates and possible explanations why motor neurons specifically show aggregate formation in patients with ALS. Stay tuned!

Michael Tibshirani

McGill University

"Parkinson's Disease: Working Towards a Cure": Part 2-- Current Treatments

This is the second post from a three part series written by Andrew Greene, a graduate student at McGill University studying Parkinson's Disease.  

While a number of worthwhile treatments exist for Parkinson’s, they all target the symptoms rather than the root cause of the disease, the death of substantia nigra neurons. This is because, at least in most cases, we still don’t understand exactly why those neurons die. We’re getting closer every year though, and some of the cutting edge research that’s bringing us towards a cure will be discussed in Part 3. For now we’re limited to symptom-targeting treatments, but as we’ll see below, some of them can be quite effective.

In Part 1 we saw that the major symptoms of Parkinson’s disease are caused by the death of neurons that emit a chemical called dopamine. It’s not surprising then, that the gold standard in Parkinson’s treatment is the administration of dopamine supplements. Unfortunately dopamine taken by mouth does not reach the brain, but scientists have circumvented this problem by using a chemical called Levodopa, or L-dopa for short. L-dopa is a natural molecule found in both animals and plants. In humans and other animals, L-dopa taken by mouth can easily reach the brain, where it is converted into dopamine. Supplementing a patient’s brain with dopamine in this manner allows them to move much more readily than they could without treatment, but there are side effects. Whereas the brain administers dopamine to itself in a carefully regulated manner, the levels of dopamine produced from L-dopa are much less finely tuned. A frequent side effect of the treatment is ‘too much movement,’ with patients making involuntary movements such as writhing or jerking. Fortunately these can usually be minimized by reducing the L-dopa dose.

When medications aren't cutting it, eligible patients can opt for various types of surgery. Like the currently available medications, the surgeries do little to block the root cause of the disease, but they can be very effective in eliminating many of the more debilitating symptoms. An increasingly common option is the implantation of a deep brain stimulation device. Somewhat counter intuitively, the net effect of the deep brain stimulation used to treat Parkinson’s is actually to block the neural activity in a certain section of the brain. This effectively inhibits the indirect pathway, which, as mentioned in Part 1, is involved in inhibiting movement and is overactive in Parkinson’s disease. Deep brain stimulation is effective against symptoms such as rigidity and slowness of movement, and is less prone to causing involuntary movements than L-dopa is. Unfortunately it’s expensive and demands a tremendous amount of expertise in medical imaging, surgery, neurophysiology, and postoperative management, thus limiting its widespread availability. Moreover, because neither deep brain stimulation nor L-dopa treatment target the cause of Parkinson’s, neurons continue to die as the disease progresses. This means that symptoms that don’t respond to the above therapies, such as cognitive problems and frequent falls, continue to worsen. For this reason, Parkinson’s disease remains an active field of research in neuroscience.

Stay tuned for Part 3: Towards a Cure. Coming soon!