The radical organization whose supposed mission is to protect animal welfare now says that cow milk not only worsens autistic symptoms but can actually cause autism too. PETA’s campaign to stop people from using animal products latched on to obscure studies of dietary influences on autistic symptoms. A PETA blog post refers to two studies that found a link between autistic children’s behavior and consumption of cow milk (or proteins found in cow milk), and jumps to conclude that "dairy foods may worsen or even cause autism.”
There’s an article in New York Times Magazine about using electrical signals in the nervous system to signal to the rest of the body to somehow alter molecular signaling outside the nervous system. Neuroscientists have known for a while that neurons transmit messages by electro-chemical signals: at each synapse, an electrical impulse arrives from a cell body, is converted to a chemical message via neurotransmitters. The chemical message jumps across the synapse, where it is again converted into an electrical signal at the next (postsynaptic) neuron. For some reason though, the thought that electrical signals interact with non-nervous system elements (like the immune system) has not been very popular; the idea that one could manipulate the electrical signals to “hijack” downstream molecular signaling without affecting neural communication itself seems like magic.
Preparing for SfN 2011, I have to give a shout-out to one of the coolest emerging technologies in neuroscience, optogenetics. Optogenetics, as everyone no doubt knows by now, is a method that allows researchers to control the electrical activity of neurons using light. Scientists infect certain types of neurons with an algae transmembrane channel protein that allows the flow of ions into a cell when light of preferred wavelength shines upon it. The method has been described well elsewhere (Steve Ramirez waxes poetic about it on the Mind the Gap Junction blog). Optogenetics is an amazing method for many reasons, but mainly because by allowing us to directly activate or silence neurons, it makes it possible to establish causal relationships in neural circuits: if neuron A is hyperactive, the mouse runs around in circles; if A is silenced, perhaps the mouse is unable to run in circles; therefore, activity in neuron A causes the mouse to run in circles. This is important because traditional electrophysiological methods allow us to only record activity without manipulating it directly (stimulating electrodes are rather crude spatially), and the methods that did allow us to manipulate activity (i.e. pharmacology or stimulating electrodes) have a myriad of effects that make precise causes of behavior unclear (i.e. does TTX act only on sodium channels? Which types? etc).
As optogenetics becomes more and more refined and widespread, I can't help to wonder what it will do for the most prevalent of neurological diseases. Will this method cure Alzheimer's? How about Parkinson's? Optogenetics promises to show us circuit-level interactions among neurons and perhaps even to nail down the network effects of particular diseases. But if we're looking to find cures for diseases instead of just fixes, we ought to not forget our molecular biologists and maybe even geneticists. That's not to say that treatments for neurological diseases are worthless! There are, after all, no cures for any brain diseases so far - so anything will be useful. With all this enthusiasm over optogenetics, we have to be honest about its capabilities and limitations.