Author: Joanna Ciafone

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Annie Derry

Ageing: Can our attitude affect our healthy life expectancy?

by Annie Derry

Nobody wants to get older, but ageing is a fact of life. Nearly everyone tries to combat its effects, whether it’s by eating superfoods or buying anti-wrinkle cream. However, there are some age-related diseases that seem to be unavoidable due to our lifestyle or our genes.

As life expectancy increases due to better healthcare, so does the proportion of older people (usually medically defined as those over 65 years old) within the population. Studies about how older people are viewed and attitudes towards ageing have never been more relevant, and some studies have found that a positive attitude towards ageing can have substantial impact on health and life expectancy.

Normal healthy ageing, or ageing processes that occur without the interruption of disease, are an inevitable part of life. These are the processes that cause greying hair, weakened joints and gradual cognitive decline amongst other things. We are still learning about ageing. It was thought until relatively recently that the neurons in our brain die as we grow older; however, it has become apparent that, without the presence of pathologies like Alzheimer’s disease, our brain cells remain almost totally intact until we die. This suggests that our cognitive capabilities should also remain, and studies have shown that we tend to assume our brain function is worse than it really is as we age.

Ageing stereotypes – fact or fiction?

It is understandable that as we grow to know more about ageing processes and diseases that we tend to focus more on the negatives. Studies such as the Longitudinal Ageing Study have been working to address these perceptions. The study suggests that, in general, members of the public tend to believe that older people are unhappier, lonelier and have fewer social interactions than they do in reality.

It seems that the stigmas associated with old age leave us with a skewed impression of how older people feel about their life situation. It has actually been found that older people are more satisfied, fulfilled, emotionally stable and more able to handle complex situations than younger counterparts!

Image source: Pixabay, https://pixabay.com/en/people-old-man-woman-couple-love-2583943/

Attitude vs outcome

It is quite well accepted that a good attitude towards life in general is thought to have a positive impact on a person’s health and well-being. It seems that this becomes of particular importance as a person grows older. This is mainly due to the fact that people who think and act like they are younger than their age are more likely to be physically active and engage in more social situations than a person who views themselves as “too old”.

An example of how such attitudes can affect health is when men experience premature baldness. Baldness is a trait associated with ageing, and in a study conducted by Ellen Langer, a Harvard professor, it was found that men experiencing premature baldness had a higher incidence of age-related health problems than men without this issue. This suggests that these men might feel older than they really are, and that the feeling of premature ageing could lead to more age-related issues. Langer also found that people whose partners are significantly older than themselves tend to experience age-related health problems at a younger age. The same study suggests the opposite is true for people with younger spouses. This indicates that a younger lifestyle may help to combat the effects of ageing for longer.

There is still so much to explore in relation to healthy ageing and combatting cognitive and physical decline. Unfortunately, some of us will always be susceptible to age-related disease according to our genes and the influence of our environment. A positive attitude towards ageing cannot stop the process. However, there is definite evidence to suggest that positive thinking towards our impending older years have the potential to increase our quality of life. Positivity can act as a self-fulfilling prophecy to help us to be happier and healthier for longer.

Interested in learning more? This blog post was based on:

André Aleman – Our Ageing Brain
The Longitudinal Aging Study Amsterdam
“Good news about the ageing brain”

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Joseph Smith

The New Neuron: one piece of a very complicated puzzle

Image source: https://pixabay.com/en/nerves-cells-dendrites-sepia-346928/

by Joseph Smith

How does the human brain work?

This question has fascinated and baffled scientists for centuries and, unsurprisingly, has led to a myriad of equally complex questions. In order to elucidate how the human brain works, it is crucial that we first understand the physiological processes that underlie its function, at a cellular level. Despite decades under intense scientific scrutiny little progress has been made in characterising the different subtypes of neuron, the cells responsible for neurological signaling, present in the human brain. However, by using advanced sequencing methodologies, neuroscientists are starting to unravel this diverse and tangled network. A small but significant piece of this puzzle has been solved with the discovery of a new neuron, the rosehip cell.

The rosehip cell

Recently, an international team of researchers combined physiological and transcriptomic analyses with the view of characterising the different cells present in the human brain. Firstly, tissue was collected from two donated human brains that had been cryogenically preserved. Individual nuclei were then extracted from neurons within the tissue and their transcriptomes analysed by RNA sequencing. By analysing the transcriptome of a cell you can find out which genes that cell expresses, as although every cell contains the same DNA they do not necessarily utilise all of the genes that their DNA encodes. In total researchers sequenced the transcriptomes of 769 nuclei before grouping them into different subtypes based on the genes that they expressed. Of the 16 subtypes identified, 11 were inhibitory, 1 was excitatory, and 4 were non-neuronal cells.

Concomitantly, researchers analysed the morphology and physiology of live cells using tissue from brain surgery and identified a neuron unlike any that had been previously described. Morphologically, these cells were larger than others and had rosehip-shaped bodies, hence the name. Notably, when researchers compared the expression profile of these cells to the previously identified transcriptomic subtypes, they found a match. Rosehip cells were found to express a number of genes associated with axon growth and synapse function. Moreover, rosehip cells were found to be physiologically distinct, and appear to function as inhibitory neurons that control transmission of information between different areas of the brain. Amazingly, when researchers compared the transcriptomic profile of rosehip cells to that of neurons found in mice they were unable to find any cells resembling the newly identified subtype. These data suggest that the rosehip cell is unique to humans.

What are the implications?

This study highlights the power of combining morphophysiological and transcriptomic analyses and identifies a new neuron with distinct properties. Furthermore, the rosehip cell is likely unique to humans; this is particularly important as, due to a lack of available human samples, the majority of studies into neuron function use mice as a model system. Fortunately, transcriptomics can be applied to tissue that has been cryogenically preserved. By continuing to characterise neurons in this way researchers may eventually be able to compare all of the different neuronal subtypes in the human brain and in doing so better understand network function pathology.

In answer to the question “how does the human brain work?” the most accurate answer is probably, “we’re working on it!”.

Want to learn more? This post was based on the Nature Neuroscience paper by Boldog and colleagues found here.

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Leonie Schittenhelm

How to ace your first conference

by Leonie Schittenhelm

Image source: https://pixabay.com/de/ereignis-auditorium-konferenz-1597531/

Scientific conferences are really cool. They just are. I mean, a ton of people interested in the same stuff you’re interested in coming together to talk about said stuff all day long? And you get snacks in between? Sign me up. But scientific conferences are also fraught with feelings of stress and insecurity – What if everyone thinks that question I want to ask is really dumb? What if my poster doesn’t measure up to what everyone else shows? How do I network with that one expert in my field, when I’m pretty sure I’ll stumble over my words because of how in awe I’m of her work? These are all hard questions.

I’m going to be really honest with you people here: I definitely did not ace my first conference. Or my second for that matter. I definitely had a problem with mostly talking to people I already knew. And I was most definitely too timid to ask a question while leaders in their fields were sitting all around me. But how do you get over that kind of stuff? And how do you ace your first (or second or fifth) conference? Here some suggestions, tested and approved by PhD students older and wiser than me. But whether you are an undergraduate student just looking to have a first whiff of the world of scientific conferences or an experienced Postdoc, conferences should be about learning new things from a variety of people and in turn let them learn from you. And eat copious amounts of snacks provided of course.

  1. Talk to people – I personally hate the word networking, but forcing yourself out of your comfort zone and chatting to a ton of new people can be really beneficial for your science. But collaborations and idea sharing aside, you shouldn’t only talk to people that you think will be somehow “useful” to you in the future. Sometimes it’s just a nice chat about the weather with a PhD student from across the country or asking one of the sponsors about their products that can make all the difference.
  2. Get active – A great way to speak to a lot of people is to volunteer some of your time at the conference to help out. Offering to be the mike runner during question time or helping to set up the presentation before the session might not only ingratiate you with the conference organisers – and potentially even shave off a couple of dollars of your registration fee – it also gives you great opportunity to chat with the speakers and other conference participants.
  3. Make sure you do your reading – Especially in bigger conferences, several sessions run at the same time, leaving you with the responsibility to make an informed decision as to which one will be the most interesting to you. Plus, by reading up a bit on the science of the session you like the most you will benefit from the little boost in background knowledge and can hit the ground running. And if you really want to talk to that one person specifically, google them and check if they published anything recently so you can chat to them about it.
  4. Review your notes – This is especially important if your hand-writing skills are as scraggly as mine. Reviewing your notes from the talks will bring back what you thought was so interesting about them in the first place and make sure you can go back to these records even in a year’s time when something clicks into place for you.

Caught the conference bug but don’t know where to start? Why don’t you sign up to Newcastle’s very own NEPG 2018 (North Eastern Postgraduate Conference) and check it out for yourself – it hits off on the 9th of November, but online registration is now open!

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Liza Olkhova

Cell replacement therapy – a hope for treating Parkinson’s disease

by Liza Olkhova 

Parkinson’s disease is the second most common disorder resulting in neuronal cell death following Alzheimer’s disease, and arises from the loss of dopaminergic cells in the midbrain. So far, treatment strategies have focused on replenishing the lost dopamine to improve patients’ motor symptoms such as resting tremor and muscle stiffness. These medications, however, may result in unpleasant side-effects.

Pluripotent stem cells are capable of differentiating into many different cell types, such as neurons, cardiac cells, etc. Generation of induced pluripotent stem cells (iPSCs) from adult cells, such as fibroblasts, and their subsequent differentiation into dopaminergic progenitor cells has been achieved at the Center for iPS Cell Research and Application (CiRA), Kyoto University. This technology would give a hope to not only compensate for a decreased dopamine neurotransmission, but to actually replenish the number of neurons that generate this neurotransmitter in the area of the brain affected in Parkinson’s.

Researchers at Kyoto University injected iPSCs-derived dopaminergic progenitor cells in the brains of macaques that were previously treated with a neurotoxin that causes Parkinson’s-like motor features. The grafted cells were not only able to survive, but to grow out its projections into other brain regions involved in movement. This led to amelioration of primate’s reduced motor functioning.

Image source: Kyoto University Center for iPS cell Research and Application (CiRA)

On the 1st of August 2018, a human Phase I/II trial was started in Japan to test the safety and efficacy of these cells in seven Parkinson’s disease patients by injecting the same brain region, called the putamen, with approximately five million iPSCs-derived dopaminergic progenitor cells (image). The cells will be injected into the putamen on both sides of the brain using stereotaxic equipment. Patients will be observed for two years during this trial and will be given immunosuppressant therapy in the case of transplant rejection.

The major concern surrounding such cell replacement therapies is a possibility of cells becoming tumorigenic; however, the original study reported no tumours formed in the macaque brain over the two-year time frame.

Cell replacement therapy could hold a promising potential to become a cure for Parkinson’s disease by directly restoring the dopaminergic neurons lost from the brains of patients, provided that clinical trials can prove the method’s safety and efficacy.

Please check out the following links for more information:
“‘Reprogrammed’ stem cells to be tested in people with Parkinson’s”
“Human iPS cell-derived dopaminergic neurons function in a primate Parkinson’s disease model”

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Emma Kampouraki

A team in synergy

by Emma Kampouraki

You should know {react} by now. If you are reading this, you’ve seen the magazine somewhere on campus, online, or you are even a fan of our blog. Be that as it may, you should have realized what {react} is trying to add to your everyday lives; a splash of science mixed with attractive design and high quality of photos.

But how did we end up there? Well, that’s an interesting story because no one is greatly confident to answer. {react} was born from a team of PhD students and a few members of staff who dreamed of a science magazine that would target a wide range of audiences, help people learn more about science, and most of all encourage students write more about science and the process of publication. {react} was soon much appreciated by the student community and, although this fluctuates, {react} often seems unable to accommodate the numerous interesting articles it receives for every issue. Then, the blog was created. It would be a pity for those articles to stay hidden in a hard drive.

A magazine would never come together without the co-operation of a big team that literally does everything from scratch. If you look at previous issues of {react}, the style slightly changes to reflect the influence of new members in the design team as well as popular demand for certain types of articles (such as research articles, as opposed to interviews). A large part of the character of {react} is its design. Another important bit is the articles themselves. And how these end up in print, is a long story.

To cut this story short, the call for proposals is announced by the team via social media, posters across campus, word of mouth and e-mail newsletters. When the deadline closes and according to the number of submissions received, we normally go through the process of reviewing the 150-word proposals and selecting the ones that reach our standards in terms of quality and fit with the pre-announced theme. Authors are then contacted with clear guidelines on how to produce their full-length articles. A sub-editor is allocated who can guide them through the process of reviewing the article and making the necessary changes to meet our publication standards. The design team comes last to format the magazine in such way that will be appealing to reach and enjoyable to read.

As in every team, we need a proper hierarchy system to ensure all needs are met within certain timeframes. This also ensures that messages are properly communicated and tasks are co-ordinated. The editor(s) organize the meetings and provide the team with guidelines and information. At the same time, the team makes decisions democratically. Positions in the committee include the sub-editors, the blog manager(s), the design team, the copy editor and the editor(s). These roles are allocated on a voluntary, first come, first serve basis during our recruitment events or training workshops. PhD students are preferred for the committee due to the nature of the magazine and to offer training opportunities for skills development; however, we have had Master students help out as well.

Issue 11 has just been published and will be available soon, both online and in print, available across campus and at most major student spots in Newcastle. It is the result of hard work, team effort and co-ordination of a great number of authors, reviewers and sub-editors. We couldn’t be prouder for this issue as it encompasses a variety of scientific topicsfrom different fields, which makes it more inclusive than ever. Join us in our training events to learn more about the magazine and, if you fancy, join our team to help bring science closer to the many audiences {react} targets and to celebrate the results of team work by a team of PhD students.

  • Current call for proposals ongoing under theme “Limits”, deadline 14th September, 150-word article proposal to be sent to react.mag.team@gmail.com
  • Upcoming training workshops:

Meet the {react} team – 12th November 2018

Meet the team behind our student-led science magazine, and learn how you can contribute as a writer, editor or designer

{react} training day – 20th February 2019

Join us for a suite of training sessions in science writing and communication delivered by experts in the fields of public engagement, science journalism and design

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Annie Derry

Epigenetics: How the environment can affect inheritance

by Annie Derry

Since the dawn of genetics, it has been well established that characteristics are passed from parent to offspring through DNA sequences. It was thought until recently that there were rigid rules to which inheritance abided: that traits could only be passed onto offspring if they, themselves, were caused by changes to the amino acid sequence making up DNA.

This was a perfectly rational conclusion based on what we observe in nature, as phenotypes we acquire over our lifetime due to our environment do not usually affect our DNA. How would these be passed on? It seemed sort of impossible.

Enter: Epigenetics.

What had not been realised until (relatively) recently is that the DNA sequence can be altered in more ways than a change to the underlying amino acid (and nucleotide base) sequence.

Epigenetic changes are chemical alterations to the genome that result in the switching ‘on’ or ‘off’ of genes. These chemical modifications can include DNA methylation of certain areas, as well as histone modification. They essentially change how easy or hard it is for that region of DNA to be unravelled, transcribed and translated into a protein (in other words, expressed). Many factors have been found that could potentially cause epigenetic changes in the body, such as stress, physical activity and diet, and it is now thought that these changes can be inherited.

Image source: Pixabay, URL: https://pixabay.com/en/baby-feet-heart-love-mother-1527456/

Wiping the slate clean?

It was previously thought that chemical changes to the genome were accumulated over an individual’s lifetime, but that they would be removed in the process of reproduction. It is now believed that this is not the case, as changes to the epigenome seem to be able to jump the generational barrier.

A widely used example of transgenerational epigenetics is the study of the Dutch Hunger Winter (1944-45), a terrible period of starvation for the people of The Netherlands. Based on well-kept medical records, pregnant women and their offspring were studied to understand the health impact of the unique conditions they were subjected to.

The interesting observation was that differences in the timing of malnutrition during pregnancy went on to affect not only the children’s weight at birth, but their health in adulthood too. Some babies (those only affected by malnutrition in early pregnancy) went on to have above-average weight in adulthood, and even to be more prone to obesity and cardiovascular disease. Those born underweight due to malnutrition in later pregnancy remained smaller in adulthood, with lower than average obesity rates. Records even suggested that the grandchildren of those malnourished women were affected similarly. A follow up study indicated that the children – many decades after initial malnutrition in the womb – had less DNA methylation of the IGF2 (insulin-like growth factor) gene than their unaffected siblings. This gene codes for an important protein in growth, thus the results suggest that an epigenetic change had taken place and could have contributed to the growth patterns of those affected children.

This gives us a small insight into how one environmental condition might cause a chemical imprint on the epigenome of a foetus that remains for their entire life and is passed on to their children.

What does this mean for us?

This does not mean to say it is certain that every little thing we do results in a genetic imprint that we pass on to our children and subsequent generations. We don’t know yet whether smoking or eating 5 fruits and vegetables everyday will be detrimental to the health of our unborn children. However, it is now clear that some aspects of our lifestyle will cause an imprint on our genome, and that imprint might not be wiped clean when we reproduce. All this means is that we can decide to take more care of ourselves, knowing that our actions may not only affect our own bodies, but those of our offspring. That being said, the field of epigenetics is a relatively new one and there is much, much more to be understood about modes of inheritance.

Interested in learning more? This blog post was based on:
Nessa Carey – The Epigenetics Revolution
Tim Spector – Identically Different
Epigenetic inheritance and the missing heritability
Transgenerational Epigenetic Inheritance: myths and mechanisms

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Leonie Schittenhelm

Just keep watching: the science behind the common TV binge

by Leonie Schittenhelm

Who doesn’t know this situation: you had the longest day, so all you want to do is go home, plop down your bag and cuddle up for an episode of your favourite TV show before an early night. Doesn’t sound too exciting, does it? But after your first episode, you decide to watch one more, and then – the plot quickens and you just really want to make sure that one character survived the gnarly explosion – just one more. Suddenly, it’s 2am on a weeknight and you are about to assure Netflix, that yes, you are still here, and for the love of god, would they please just continue with the next episode before that latest cliff-hanger makes you die of curiosity. Those my friend, are the classic signs of a TV binge.

Just as other binges involving alcohol or food, the TV binge has moved into the focus of modern research. While the negative side effects of excessive drinking might be more immediately obvious, a team of researchers from Newcastle University, the University of Stirling and Ottawa University are arguing for the importance of investigating TV binges in their paper, ‘‘‘Just one more episode’: Frequency and theoretical correlates of television binge watching”. Not for nothing is lack of physical activity number four on the list of mortality risks worldwide, and TV watching is the most popular sedentary activity during people’s free time. But what even constitutes a binge? And how do people feel about them?

These are just some of the questions the paper tried to answer by asking 110 people about their TV watching habits. They defined a TV ‘binge’ as watching more than two consecutive episodes of the same TV show in one sitting. While this seems quite a low threshold – and embarrassingly ups my TV binges per week to above the average of 1.47 that was reported by the participants – the reason that you move from the second into the third episode is that you are likely to have switched from a conscious decision to watch TV to a zombie-like ‘keep playing’-mode. This automaticity of pressing the ‘next episode’ button was reported to be especially frustrating for the study participants: most connected their excessive TV watching with feelings of regret and indicated that it interfered with pursuing other goals important to them. While a lot more research has to be done, TV binges are a cultural phenomenon that are not going away. Until we know more, I’d better get working on my personal impulse control.

Want to know more about this study? Give it a read yourself: Walton-Pattison, Emily, Stephan U. Dombrowski, and Justin Presseau. “‘Just one more episode’: Frequency and theoretical correlates of television binge watching.” Journal of health psychology 23, no. 1 (2018): 17-24.

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Georgia Collins

Going for a Plastic-Free July!

Image from http://i.imgur.com/alT1hhO.jpg

by Georgia Collins

You may have already heard of the campaign, started in Australia in 2011 by an environmental group based in Perth, called Plastic Free July. This year the project has more than 2 million people from over 150 countries pledging to minimise their use of plastic for the month of July. There are three levels of challenge, the simplest being to eliminate all single-use non-recyclable plastic in your daily life, such as that from takeaway coffees and plastic bags. I was introduced to it by a friend, and we have both decided to take on the full challenge; we will not use any non-recyclable plastic or single use plastic for the whole of July.

To get started with Plastic Free July, we signed up with the website, http://www.plasticfreejuly.org/ and took the ‘Pesky Plastics Quiz’. This was really interesting for me as I thought I was quite aware of plastic and was already avoiding excessive packaging. However, this quiz really showed me how much single-use, non-recyclable plastic I use and, scarily, how little I had noticed.

As well as avoiding anything with plastic wrapping or single-use plastic, we’re also finding alternatives for common everyday things. For example, bin bags can be replaced with compostable or newspaper liners (although thus far we’ve managed to recycle, compost or reuse all of our “waste”). We’re also ditching yoghurt pots… did you know that making your own yoghurt is actually really easy? (Making soya yoghurt, though,… not so much!). We’re also making a concerted effort to buy from shops that sell items either unpackaged or in recyclable containers. Hopefully through such alternatives we will fix our bad-plastic-habits for good.

As I’ve never studied economics/ politics/ anything societally useful, I don’t really get why there just isn’t a ban on all plastic that cannot be reused, composted or recycled, especially when a really cool, environmentally-friendly alternative already exists! For example, take a look at Vegware. Totally amazing! I can’t get over the fact that takeaway boxes can be compostable! I recommend looking at stuff like this as a good break from the actual work you are supposed to be doing and to restore one’s faith in humanity and human innovation. It also makes a nice change from being depressed about our detrimental impact on the environment.

Currently, many privately-produced products are public-waste problems. We can all fantasize (well, maybe not ALL of us, but I do it) about companies having to adopt closed-loop systems for their packaging: can you imagine if Coca-Cola suddenly had to be responsible for their plastic bottles?! I mean ALL their plastic bottles… even all the really, really old ones currently in the sea. But Lush, a cosmetics company, have already taken the initiative and are responsible for all their packaging (just because you’re an environmentalist doesn’t mean you can’t look and smell fantastic). Although it is frustrating that most big companies aren’t responsible for the effect they have on our environment, we can’t afford to be complacent as we all have some responsibility for creating plastic waste. We need a collective change, a cultural makeover that will reach every single one of us, and that most definitely can begin at home. The Earth is all of our homes after all, and right now we are just messing it right up. We all can take some responsibility for this, and movements like Plastic Free July are such an eye-opening way of realising how little we do.

We all know what plastic does, where it ends up… everyone must have seen Blue Planet by now. We can’t say we don’t know. What we can say though is, “no thanks!” to any single-use plastic. We can bring our own take-away cups, cutlery, lunch boxes and bags, and avoid the ridiculous packaging at many shops. Rather than just shaking our heads with dismay at some ridiculously wrapped vegetable (like, shrink-wrapped coconut?!) or getting upset about whales dying from swallowing plastic bags, we can use these emotions to do something and to stop polluting with plastic. You are responsible for what you buy, so don’t buy stuff that ends up on our beaches, buried in a hole and outliving the entire human population, or getting stuck in some poor albatross.

Go on, and make a fish happy by going plastic free!

PS. As part of Plastic Free July, my friend and I are saving all the plastic that we have inadvertently obtained. The count so far is 2 pieces of plastic packaging tape, a plastic bag from some unavoidable packaging (from a new pair of goggles – the goggles were in a plastic case, then in a plastic bag, then in a padded envelope…), and a pot holding some olives bought back in June. And we are only in day 4!

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Cassie Bakshani

The legacy of Koko the gorilla


by Cassie Bakshani

Hanabi-ko, or Koko, as she was affectionately named, was a female western lowland gorilla born at San Francisco Zoo on July 4th 1971. She spent most of her life at the Gorilla Foundation in California and it was here that she died in her sleep on June 19th, 2018, at the age of 46.

Koko, an ambassador for her species, was instrumental in developing our understanding of cognition in great apes. In 1972, Stanford University graduate and developmental psychologist Francine Patterson began teaching one year old Koko American Sign Language. The infant gorilla was initially confused and reluctant, and would attempt to bite Francine when she moulded Koko’s hands into the correct configuration for a sign. However, after moving Koko away from the distractions of the zoo enclosure and introducing her to more isolated living quarters in a mobile trailer, Francine reported that Koko was acquiring new signs at a rate of one sign per month. By seven years old, it was estimated that Koko possessed a working vocabulary of approximately 375 signs. By the time of her death, she was able to understand more than 1,000 words.

Communicating in this way, Koko provided valuable insights into the minds of great apes, including their emotional capacity and information processing abilities. Researchers marvelled at her ability to express herself in a ‘humanlike’ manner, discussing her likes and dislikes using aspects of our own language and demonstrating empathy within interspecies relationships. Notably with an adopted kitten named All Ball, with whom she developed a close maternal bond, she displayed behaviours we associate with grieving upon learning of his death, signing the words ‘bad, sad, bad, frown, cry-frown, sad’.

Koko provided an example of how our closest living primate relatives rely on complex social interactions to navigate through daily life. Nevertheless, whilst scientists learnt a great deal from studying Koko, it is important to recognise the sacrifice she was required to make to her everyday existence purely to fulfil our scientific curiosity. The ethics associated with confining an intelligent animal in unnatural conditions are concerning, particularly, as in Koko’s case, where she was largely unable to communicate with others of her own kind, let alone in the social group-settings observed in wild gorilla families.

Koko’s impact will undoubtedly be long-lasting and it is my hope that we reflect on this experience and allow it to inform how we, as scientists, study animals in the future. We have a duty to ensure focus on not only our intellectual gain, but also on the physical and psychological wellbeing of these incredible animals.