Scientific Cafe 2012: Brain Myths

Last night was BAW's first Scientific Café of 2012, with the topic being "Brain Myths," a topic that I've written about before, and the discussion of which I feel is crucial in dispelling popular misconceptions regarding the brain and its functions as well as being particularly suited to the Café’s general audience.

The guest speakers were Dr. Ed Ruthazer (McGill; Montreal Neurological Institute), Dr. Natasha Rajah (McGill; Douglas Institute), Dr. Michael Fehlings (University of Toronto), and Dr. David Ragsdale (McGill; MNI). I'll provide a quick recap of the topics covered by each of the guests along with some of my own comments.

Dr. Ruthazer focused primarily on experience and perception, and how these originate within the brain. Recent advances in technology have allowed us to make incredible leaps in our understanding of perception; in particular, it's possible to reconstruct one's visual experience using imaging techniques, albeit with (currently) limited accuracy and resolution. As technology advances, it will increasingly become possible to reconstruct one's experiences through analysis of brain activity. Future technology may also lead to a complicated (but fascinating) ethical and philosophical issue: if consciousness is an epiphenomenon of brain activity, and we eventually become capable of producing sophisticated artificial 'brains', what are the consequences of producing artificial intelligence and sentience that mimics or rivals our own?

Dr. Rajah focused on myths related to memory. One common misconception is that our brains act as 'recorders' that faithfully encode events for subsequent accurate retrieval. However, work from Dr. Elizabeth Loftus and others has shown that our own memories are in fact rather fallible, in that memories can be modulated or even (in some cases) inserted, with the manipulated individual confident that their adulterated memories are both accurate and their own. In fact, stating that we believe something reinforces that belief, leading to false confidence in a fallible memory if it is declared often enough. Similarly, repressed memories are controversial in this field, with the general consensus being that traumatic events would normally be remembered to some extent, and that repressed memories are likely to be false memories. Finally, myths regarding memory loss in popular media can be misleading, as common misconceptions regarding amnesia are produced from inaccurate fiction.

Dr. Fehlings lamented the fact that there are very few examples of clinical neuroscientists or neurosurgeons in popular fiction (with Dr. Frankenstein, or his younger Mel Brooks equivalent, as rare examples). In the scientific world, however, we are rapidly gaining an understanding of brain regeneration and repair following injury. One example he mentioned is adult neurogenesis, which I've previously written about here, as well as the therapeutic potential of implanted neural stem cells. In closing, he stressed the importance of translational research, in which new insight into brain repair and regeneration gleaned from basic science is applied at a clinical level to patients of neurotrauma.

Finally, Dr. Ragsdale focused on more philosophical concerns related to neuroscience. In particular, if the mind is an epiphenomenon of brain activity, what is the mechanism by which this occurs? If our consciousness is a product of deterministic forces (i.e. underlying neurobiology and its features), do we actually have free will? One experiment exploring the latter described how the neural activity underlying a voluntary action actually precedes the conscious decision to perform the action by roughly a half-second. So if our brains are making our decisions for us, is free will an illusion? He concluded with the importance of creative thinking in neuroscience research, in that our understanding of our brain is still very incomplete, and so there is still lots of room for wild new ideas about the brain to lead to insight about ourselves.

If you couldn't make it to the event, I hope this provided a rough explanation of the type of topics covered. I would definitely recommend checking out any future Science Cafés, as they're stimulating and worthwhile events that make complicated topics accessible to a general audience.

New neurons and a new therapeutic target

The recent discovery that the human brain produces new neurons throughout life has led us to re-evaluate how we think about our brains and their plasticity, as well as examine potential new targets for psychiatric treatment.

In the narrow space between your ears, a roughly three-pound lump of tissue (composed mostly of water) contains everything that makes you who you are. Your brain is responsible for all of your memories, emotions, actions and aspirations. The human brain is also the source of all of our joy and misery, and understanding its workings offers hope for the amelioration of psychiatric suffering and, possibly, greater potential for happiness and enjoyment of life. However, one difficulty in dealing with the complexity of psychiatric disorders is that frequently multiple theories arise to help explain the origin or cause of any particular condition. 

Depression is one example of this; there are many hypotheses attempting to explain this debilitating condition that affects more than 120 million people worldwide. One of the most widely-known theories is the 'monoaminergic theory' of depression, which focuses on neurotransmitters (chemicals used by neurons for communication) like serotonin. However, in this article I will try to give a brief review of a more recent theory, the 'neurogenic theory' of depression.

Up until relatively recently, it was believed that the brain stopped producing new neurons after development; as the famous neuroscientist Santiago Ramon y Cajal said around a century ago, "In the adult centers, the nerve paths are something fixed, and immutable: everything may die, nothing may be regenerated". However, the creation of new neurons in the mature brain, a process known as 'adult neurogenesis', was confirmed relatively recently in humans.

But there are some mysterious aspects to this phenomenon. For one thing, there initially seems to be only two clearly neurogenic areas in the brain; the olfactory bulb, and the dentate gyrus of the hippocampus. There's some early evidence to suggest other parts of the brain may be neurogenic as well, but even in these areas, the number of new cells produced seems to be limited at best. So this raises some questions; why just these few areas in particular, and not others? And what is the function of these new cells?

Although adult neurogenesis is still a relatively new discovery, it's become something of a hot topic in neuroscience, so we have some preliminary answers to the questions I just posed. For one thing, these new neurons seem to have special properties, in that immature neurons seem more 'plastic' or flexible in their firing responses than other cells. We also have some hints at their function, particularly with hippocampal neurogenesis; it's been shown to be involved in learning and memory and, most importantly for this entry, has been associated with emotional functioning.

This brings us back to the neurogenic theory of depression, an idea that essentially states that if the rate of production of these new 'special' neurons decreases, depressive symptoms may appear or be increased in severity, whereas increases in the rate of adult hippocampal neurogenesis can reduce the severity or appearance of depressive symptoms. Although this idea is only a few years old, there's some evidence supporting it. For one thing, factors that seem to make depression worse, such as stress, also decrease hippocampal neurogenesis, and factors that have been shown to improve depressive symptoms, such as antidepressant drugs and electroconvulsive treatment, also increase hippocampal neurogenesis. Human depressed patients also show decreased volume of the hippocampus. In addition, the delay between starting antidepressant medication and the amelioration of depressive symptoms, roughly four to six weeks, closely mirrors the time necessary for newly-proliferated cells spurred by this medicine to develop into functional neurons. And finally, experiments using animal models have shown that factors that increase neurogenesis also induce antidepressant behaviour.

So the neurogenic theory of depression, although it's still a relatively new idea, has the potential to offer exciting insight into depression and other psychiatric conditions, including treatment applications; if increasing the rate of neurogenesis can improve depression and depressive symptoms, then we can potentially develop new medications and treatments aimed specifically at increasing adult neurogenesis.

It's important to keep in mind that a lot of the theories scientists have developed concerning psychiatric illness are still preliminary, and a lot of important research is still needed before we can provide the definitive answers patients and their families are desperate to hear. However, the silver lining is that we're constantly getting closer to finding those answers, and offering hope to those searching for it.

- Ian Mahar

[Adapted from an article initially published here]