Although chemical and biological warfare has been internationally condemned since the 1600s, scientific research has continued to uncover chemicals which can have a devastating effect on the nervous system. Indeed, at the end of last year there were reports of an alleged government attack on civilians using an unidentified nerve gas in the city of Homs in Syria. It is thought that Assad’s regime have been developing and stockpiling chemical weapons. If this is true, the situation shows disturbing similarity to Saddam Hussein’s use of the nerve gases against Iranian civilians during the Gulf War in the 1980s.
Interestingly, the discovery of nerve gases was made more or less by accident. The organophosphate (OP) family of nerve gases, including sarin and tabun, were being studied by German scientist Dr. Gerhard Schrader during the 1930s as possible insecticides. Whilst studying these chemicals Dr. Schrader accidentally spilled a drop of tabun onto the bench and, within minutes, was overwhelmed with dizziness and had difficulty breathing. It took him and his colleague three weeks to fully recover from this exposure.
OP nerve gases work by stopping the enzyme acetylcholinesterase (AChE) from breaking down the neurotransmitter acetylcholine (ACh). Normally, when ACh is released by nerve cells it is rapidly broken down by AChE, meaning that it can’t build up around target cells. However, when AChE stops working ACh collects around cells, overstimulating them. The effects are often seen as over-stimulation of muscle cells and glands which produce bodily fluids. After very high exposure to OP a victim will suffer a huge number of horrible symptoms, including, a runny nose, tight chest, blurred vision, shortness of breath, nausea, muscle spasms, drooling, crying, incontinence, vomiting and abdominal pain. In this case, death usually follows quickly, either due to choking or from suffocation caused by overstimulation of the diaphragm. Sarin was infamously used by the Japanese terrorist group Aum in an attack in a Tokyo subway station in 1995, which killed 13 and left thousands with temporary vision problems.
Another family of chemicals that affect the nervous system are anti-cholinergics. Anticholinergics stop ACh from activating receptors on target cell (muscles and glands). As a result, these chemicals have almost entirely the opposite effect to OP nerve gases. The symptoms include a dry mouth, muscle weakness, blurred vision, as well as hallucinations and some pretty strange delirious behaviour. Anticholinergics could have a potential (though still illegal) use as a ‘non-lethal’ weapon to incapacitate people – since people can’t really fight back if they’re delirious. Saddam Hussein was accused of stockpiling the anticholinergic Agent 15 to use in the Persian Gulf War against Kurds and Iranians. Another similar chemical known as BZ was weaponised by the U.S. military during the Cold War. Thankfully, stocks were uncovered and destroyed before it was deployed. BZ was also discovered by accident by a scientist innocently working on digestive disorders.
Despite some of these examples, where dangerous biological weaponry has emerged from otherwise benign research; there would be no sense in avoiding all scientific research in the fear that someone might accidentally stumble across the next weapon of mass destruction. Scientists certainly have a duty to be aware of the potential uses for their work, especially since research is (or should be) freely accessible online. However, ceasing research into potentially hazardous chemicals altogether would inhibit some pretty important discoveries; especially since many chemicals which are beneficial in small doses, could have a lethal ‘dual-use’. Indeed, drugs which inhibit AChE are not just potential biological weapons, they are also currently the most widely used treatment for Alzheimer’s disease.
Perhaps, since the discovery of the occasional nasty seems unavoidable if important biological research is to continue, the best course of action would be to fund counter research into possible treatments.
At the University of Sheffield, Prof. Mike Blackburn and his collaborators have recently developed a ‘bioscavenger’ to mop up OP chemicals, preventing them from attaching to AChE. This kind of treatment will hopefully help save lives in the event of nerve agent attacks. Last year, Dr. Moshe Goldsmith at the Weizmann Institute in Israel mutated a human liver enzyme so that it could break down OP nerve gas molecules. While this research holds obvious benefits to humanity, the implications of this work also raises an ethical dilemma. If the gene code for this newly-evolved enzyme could be put into soliders, we could be faced with a scenario where armies can be genetically manipulated to become immune to chemical or biological weapons. Unfortunately, this hypothetically amazing feat of science could result in an biological arms race…a situation it’s hard to envisage anyone winning.
The Arts and Humanities Research Council has a Neuroscience Ethics Network that bring together researchers from all over the UK. Some of this article has been based on prospective lectures initiated by the Network, intended for undergraduate Neuroscience students. If you’d like to read more about the Network, please click here: http://www.lab.ls.manchester.ac.uk/neuroethicseducation/
Post by Natasha Bray
In order to find the ‘social’ or ‘friend’ centre of the brain, scientists measured the size of different brain structures associated with making and maintaining friendships. In two different studies, they found that the size of an individual’s amygdala (the emotional centre of the brain) and their orbital prefrontal cortex (oPFC) were proportional to the number of real friends and social groups they had. In other words either having a larger amygdala or oPFC means you are more likely to be friendlier, or the more friends you ‘add’ to your social network, the larger those parts of the brain become. In fact, it’s probably a mix of both situations.
Robert Dunbar, a British anthropologist interested in the evolution of society, also attempted to define how the structure of the brain linked to the size of an individual’s social group: the equivalent to the average Facebook friend count. His early work focused on the brains of various species of monkey. From this work he found that he could predict the size of the animal’s social group from the size of their neocortex compared to the rest of their brain. He discovered that primate species which have a larger neocortex relative to the rest of the brain hang out in larger social groups, whereas those with a smaller neocortex have fewer ‘friends’. These monkeys’ brains have either evolved or changed to maintain friendships with a certain average number of other monkeys. From this Dunbar was able to predict that, if humans are like monkeys (which we are), our neocortex:brain ratio predicts that we should be cliquing into social groups of around 147.8 (with an upper limit of 300). What’s interesting is that this is essentially the case in real life: 150 is the average size of a tribal village, the optimum size in the Roman army’s military unit and the average number of friends on Facebook is actually creepily close too.
Whether or not we realise it, most of us are hard-wired to seek out friendship. Our brains are social and we have evolved to cooperate and share – that’s why Facebook is such a massive phenomenon. But what does the size of our ‘friends’ section say about us? In a very modern experiment, psychologists asked people to rate another person’s attractiveness based on a fictional Facebook profile. These profiles were identical other than one factor: for each profile the experimenters altered the number of friends these fictional people had, either 103, 303, 503 or 703. These experiments found that 303 seemed to be the magic number, with participants rating profiles with this number of friends as being most ‘attractive’. Perhaps this could be a reflection of the upper limit of Dunbar’s number. Interestingly, both profiles with lower and higher friend counts were rated as being less attractive. Perhaps fewer friends is taken as an indication that a person is less sociable, whilst having too many friends may be seen as ‘trying too hard’. So when honing your online persona it’s more than just the pictures of that dodgy night out you have to worry about.
But there are many more important benefits from having a strong, optimally-sized social group. Researchers in Kenya watched wild baboons to see how long higher socially ranking males and lower socially ranking males took to heal or recover from naturally occurring injuries and illnesses. Despite the highest and lowest ranked baboons experiencing a similar amount of biological stress, the lower-ranked baboons took an average of six days longer to heal or recover than alpha males. The researchers think this could be due to the positive impact that close friendships have on the immune and repair systems.
This rift is exemplified by the shocking fact that there is only one British Member of Parliament out of 650 that has a scientific, research-based PhD (Lib Dem MP for Cambridge Julian Huppert, Biological Chemistry, in case you’re wondering). Similarly in the United States, 3 in 435 people in the House of Representatives have a non-medical, scientific background. And considering Prof. Nutt’s dismissal, it seems that scientists are seen by politicians as commodity experts whose advice can be cherry-picked for a bit of ‘policy-based evidence-making’. Winston Churchill once said that science should be ‘on tap but not on top’. But what’s stopping us scientists from getting properly involved in politics?
The main thing scientists have got going for them if they fancy residing in Downing Street is the doctrine of science itself. As Carl Sagan (the American Brian Cox of his time) said, “science is a way of thinking much more than it is a body of knowledge”. The knowledge bit isn’t bad either and it lasts far beyond the sell-by date of parties’ policies. The logic that underlies the analysis of data gathered from random, blinded, controlled trials is the perfect way of objectively testing different policies. And we’ve got buckets of that logic to share with our MPs.
Earlier this year, Edwin Hart Turner (38) was executed by lethal injection after being convicted of murdering Eddie Brooks and Everett Curry in a robbing spree near Mississippi. Shortly before the murders, Turner had been admitted at a mental hospital for depression after an attempted suicide. The defence attorneys’ main argument against Turner’s execution was his unstable state of mental health. Guilty or not guilty, Turner’s lawyers argued that a mentally ill person should be exempt from state execution.
Admittedly, cases such as these aren’t exactly common. However, with further advances in our understanding of mental illness these stories are increasingly relevant, necessitating a level of crossover between neuroscience and legal ethics. This crossover poses a major dilemma for society, the question of how much personal control we have over our own brains and whether or not we can be held entirely responsible for our actions? Must all mass-murderers be, to some extent, mentally ill since they fall so far outside a ‘normal’ moral spectrum? Are we less accountable for our actions and decisions since our brains’ functions are a product of our biology and social influences?
At the end of 2011 The Royal Society published a report stating that in the USA, neurological or behavioural genetics were used as evidence for 722 legal defences between 2005 and 2009. In Italy, a woman had her sentence for murdering her sister reduced after the defence lawyers presented genetic and imaging evidence that her brain’s anatomy was different to that of 10 normal women. On the other hand, in 2008 an Indian woman was convicted of poisoning her husband when a scan of brain activity allegedly revealed that she had knowledge of events surrounding her spouses death which could only have been gained through experience. Neuroscientists are now often called upon as expert witnesses and so should have a understanding of the legal and ethical implications of their testimonies.
So what does this mean in real life? Today, it is estimated that 90% of UK prisoners have a diagnosable mental illness or substance abuse problem (Office for national statistics). About 1 in 7 of all prisoners in the UK are thought to have four concurrent mental health problems, often not simply associated with the time spent in prison. Also more than half the reported prisoners who commit suicide in prison exhibit symptoms of mental health problems on entering prison. Whether or not these mental health issues preceded or even contributed to their crime is unknown (and I can’t say how one would ever prove that beyond reasonable doubt), but I think that this has huge implications for the prison system. Seeing as people outside prison with mental illnesses are treated as patients rather than criminals, I think the government should focus on treating and rehabilitating, rather than punishing, prisoners who have been incarcerated on their brain’s behalf.
with flies. First install the DNA for a phototrigger system into neurons at the base of a fly’s wing, now from this DNA those neurons can construct their very own light-responsive receptors. These neurons become active when a light is shone on them, just like the algae. Shine a light, the neurons become active and fire, telling the wings to beat. Result: we have take-off. And just in case you’re thinking the fly just sees the light and tries to flee, the same happens in decapitated flies. Gross but true! If you want to know more or need to see it to believe it: 
When I first heard about optogenetics, I was gobsmacked at how clever and insightful the technology sounded. A small part of me was originally hesitant, however. I’ve obviously watched too many films that make me almost suspicious of a tool that could potentially enable mind control, or, dare I say it, ‘brainwashing’. Anthony Burgess’ Clockwork Orange springs to mind: “When a man cannot choose, he ceases to be a man.” (Anthony Burgess). The implications of this technology are massive and, without wanting to sound like too much of a film nerd, ‘with great power comes great responsibility’ (Spiderman, if you’re wondering). Luckily, though, after reading up on optogenetics, I’ve come round to realise that its potential for good far outweighs the fearsome idea that the technology would be used to construct an army full of mindless, Jason Bourne-esque zombies. Like I said, I watch far too many films.
There’s a spy film (I can’t remember which one) with a famous scene where the secret agent and his enemy sit down for drinks. The agent secretly slips a pill into his mouth to counter the effects of the alcoholic beverages they both proceed to consume. Throughout the rest of the night, the spy retains all his mental faculties, knowing that meanwhile his enemy will succumb to impaired judgement, delayed reflexes and slurred speech. This is all caused by the alcohol slowing down the enemy’s brain by binding onto ‘depressant’ receptors, called GABAA receptors, making them more active – in turn, slowing down the brain.
So what is the agent’s ‘magic’ pill that protected him from this dreaded sequence of events? Today the internet is full of suggestions, many herbal or vitamin-based. Not surprisingly, there is a huge market for ‘miracle’ hangover cures. Yet hardly any claim to be able to curb the primary effects of alcohol – feeling ‘drunk’. Recently, however, scientists at the University of California have tested a natural substance called DHM (taken from an Asian tree) on rats. The rats were given a dose of alcohol equivalent to a binge of 15-20 pints of beer. The rats that weren’t given the DHM lost their ‘flipping’ reflex (their ability to stand up after being pushed over) for over an hour. In contrast, the rats given DHM before the alcohol only lost their ‘flipping’ reflex for around 15 minutes. In other words, DHM made the rats extremely tolerant to alcohol.
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