Synaesthesia – a ‘mixing of the senses’

The 2014 winner of the Paul Bourke Award was Associate Professor Anina Rich, a researcher from Macquarie University. This honour is awarded annually by the Academy of the Social Sciences in Australia to an early researcher who has achieved excellence in their field. As part of the award the winner presents their recent research in a public lecture at their home university. Dr Anina Rich studies how the brain integrates sensory information, particularly focusing on synaesthesia.

People with synaesthesia (synaesthetes) perceive sensory information in a different way. They can experience colours in association with letters, sounds or smells. The most common type of synaesthesia is letter-colour (Figure 1) but there are also other types such as auditory-visual and olfactory-visual synaesthesia. Chiou & Rich (2014) define synaesthesia as a ‘concurrent and distinct experience in a separate or the same modality’.

Figure 1. A representation of the colours one synaesthetes associates with each letter and number.

Figure 1. A representation of the colours one synaesthete associates with each letter and number.

Synaesthesia is present is 0.05-4% of the population and may have a genetic link. Relatives with synaesthesia are common and it is more prevalent in females than males. Many people don’t realise they are a synaesthete as their synaesthetic experience is constant over time and normal for them (perception in general is subjective).

Dr Rich is interested in studying synaesthesia as it may provide information about how information is normally integrated. Synaesthesia is not a medical disorder, there are no deficits associated with it. Many synaesthetes report that the extra sensory information they receive can be used to improve their memory and learning. Dr Rich is interested in seeing if synaesthetes have extra connections in the brain or are just using their connections between brain sections in a different way to the rest of the population.

To test this idea, Dr Rich and her team asked seven auditory-visual synaesthetes to describe the location on a grid of colours and shapes in response to auditory stimulus (Figure 2). Using functional MRI, Dr Rich and her team were able to work out that the occipital lobe in the back of the brain is stimulated when auditory-visual synaesthetes are presented with auditory information.

Figure 2. Examples of the stimuli presented to the auditory-visual synaesthetes (Chiou et al. 2013).

Figure 2. Examples of the stimuli presented to the auditory-visual synaesthetes (Chiou et al. 2013).

In addition, Dr Rich’s team has been investigating the areas of the brain non-synaesthetes use to process information about objects and colours. For example, a lemon is instantly recognisable as a lemon due to its yellow colour. When this colour is changed to something incongruent, like a red lemon, it becomes harder to identify. This object-colour binding is centralised in the anterior temporal lobe of the brain. Dr Rich is now conducting research to see if the same brain location of object-colour binding is seen in synaesthetes and what happens to their synaesthetic experience if the activity of this brain region is temporarily disrupted (Chiou et al. 2014).

Studying synaesthesia and how the brain processes sensory information is important as it can provide information about how learning and experience can alter our perception. As Dr Rich said in her presentation “what we already know has huge influence on what we think we see”. This work has implications for designing environments where people are required to process multiple sources of information, such as airplane cockpits.

To learn more:

Chiou R & Rich AN (2014). The role of conceptual knowledge in understanding synaesthesia: Evaluating contemporary findings from a “hub-and-spokes” perspective. Frontiers in Psychology, 5(105), 2-18. doi:  10.3389/fpsyg.2014.00105.

Chiou R, Stelter M & Rich AN (2013). Beyond colour perception: Auditory-visual synaesthesia induces experiences of geometric objects in specific locations. Cortex, 49(6), 1750-1763.

Chiou R, Sowman PF, Etchell AC & Rich AN (2014).A Conceptual Lemon: Theta Burst Stimulation to the Left Anterior Temporal Lobe Untangles Object Representation and Its Canonical Color. Journal of Cognitive Neuroscience, 26(5) 1066-1074. doi:10.1162/jocn_a_00536.

Prevention is Better Than Cure – Keeping Dementia at Bay

What do we know about dementia?

Recently Associate Professor Michael Valenzuela spoke at Macquarie University’s Australian Advanced School of Medicine about his work with elderly Australians. Associate Professor Venezuela leads a team of researchers at the Brain and Mind Research Institute, part of the University of Sydney. His work is important for determining how elderly people can be productive into old age rather than being confined to institutions or nursing homes. Dementia is not one disease, but a collection of diseases characterised by a decline in brain functions, such as perception, memory, language and cognitive skills1. Research has shown that shrinkage of the hippocampus (a brain section important for memory and spatial skills) is an indicator for dementia (Figure 1)2.

Figure 1. Shrinkage of the hippocampus in healthy elderly people and suffers of  Alzheimer’s Disease (one of the diseases under the umbrella of dementia)2.

Figure 1. Shrinkage of the hippocampus in healthy elderly people and sufferers of Alzheimer’s Disease (one of the diseases under the umbrella of dementia)2.

What are the risk factors?

So what determines whether an elderly person can maintain an independent lifestyle or become dependent on others for care and support? A major risk factor for dementia is being mentally lazy. A person’s cognitive lifestyle across the years of their life is a major factor in the risk of cognitive decline and developing dementia as a person ages. A survey of elderly people in Australia, the UK, the USA and France (Lifetime of Experience Questionnaire) is currently being conducted to find out more about how cognitive lifestyle correlates with risk of dementia3.

One recent finding of the Lifetime of Experience Questionnaire is that managerial experience during a person’s working life is correlated to a bigger hippocampus. Managing at least 10 people can be effective at preventing the onset of dementia4. The researchers analysing the data have postulated that interactions with people and the complex skill set required to successfully perform in a management position are what leads to this reduction in dementia risk.

What can we do to stave off the onset of dementia?

The findings from Associate Professor Valenzuela’s research show that one way to reduce the risk of dementia is to maintain an active cognitive lifestyle (ACL)5. Consistently ‘working out’ your brain can increase the time you live with a clear mind and reduce the amount of time living with dementia6. This pushing back of the onset of dementia is known as compression of cognitive morbidity. Pablo Picasso is a wonderful example of a person who was active and independent into old age. He continued to paint right up to his death at 73 years old (Figure 2).

Figure 2. Pablo Picasso adding paint to an artwork.

Figure 2. Pablo Picasso adding paint to an artwork.

How do we go about promoting active cognitive lifestyles in communities?

Associate Professor Valenzuela’s team has started a Brain Training Lab at the Montefiore Home in Randwick, Sydney (Figure 3). Here the program participants undergo computer-assisted cognitive training for 60 minutes, three times a week over a 12 week program. There are two groups – one does repeated standardized tasks and the other group watches National Geographic videos and answers questions about them. This study aims to answer questions about the minimum/maximum amount of training required to improve cognitive function and how long positive effects from brain training can last7.

Figure 3. Participants undertaking computerised tasks as part of the Brain Training Lab.

Figure 3. Participants undertaking computerised tasks as part of the Brain Training Lab.

Another experiment that has been established is the Study of Mental Activity and Regular Training (SMART) trial. This study combines mental and physical training to see if either type of training in isolation or the combination of both improves cognitive abilities8. The link between exercise and brain health has been observed in rat experiments. Exercise has been shown to improve brain organisation and object/place recognition in aged rats. This link has also been demonstrated in humans; exercise training has been shown to increase the size of the hippocampus9. The SMART study includes 100 Sydneysiders over the age of 55 and they conduct training twice a week for six months. Measurements of cognitive ability before any training, after six months of training and at an 18 month follow-up hope to determine if there are improvements in the brain, general health and quality of life of the participants8.

Wider implications

Only in the past 100 years have people been able to live beyond 65 years of age. The population of the world is aging fast due to the maturing of the baby boomer generation and medical advancements extending life expectancy. The combination of aging populations and increased life expectancy means more people than ever before are soon going to be retired. Retirement design needs to be carefully considered so the development of dementia in aging population doesn’t negatively impact on the economy and health care systems10. Studies on aging and cognitive ability have shown that it isn’t effective to retire and then do no ‘brain work’ for 20-30 years. Associate Professor Valenzuela warns that retirement design needs to take this into account. Opportunities need to be created where elderly people can replace the intensive cognitive and social interactions of a work environment when they retire. Only in this way can the older people retain their cognitive abilities and stave off the onset of dementia.

Want to learn more?

  1. Department of Health, Commonwealth of Australia (2013). Dementia,, accessed 23 May 2014.
  2. Thompson PM, Hayashi KM, de Zubicaray GI, Janke AL, Rose SE, et al. (2004). Mapping hippocampal and ventricular change in Alzheimer disease. NeuroImage, 22(4), 1754-1766. doi: 10.1016/j.neuroimage.2004.03.040.
  3. Valenzuela M & Sachdev P (2007). Assessment of Complex Mental Activity Across the Lifespan: Development of the Lifetime of Experiences Questionnaire. Psychological Medicine, 37, 1015-1026. doi: 10.1017/S003329170600938X.
  4. Suo C, Leon I, Brodaty H, Trollor J, Wen W, et al. (2012). Supervisory experience at work is linked to low rate of hippocampal atrophy in late life. NeuroImage, 63, 1542-1551. doi: 10.1016/j.neuroimage.2012.08.015.
  5. Marioni RE, van den Hout A, Valenzuela MJ, Brayne C, Matthews FE, et al. (2012). Active cognitive lifestyle associates with cognitive recovery and a reduced risk of cognitive decline. J Alzheimers Dis, 28(1), 223-230. doi: 10.3233/JAD-2011-110377.
  6. Marioni RE, Valenzuela MJ, van den Hout A, Brayne C, Matthews FE (2012).Active Cognitive Lifestyle Is Associated with Positive Cognitive Health Transitions and Compression of Morbidity from Age Sixty-Five.PLoS ONE, 7(12), e50940.doi: 10.1371/journal.pone.0050940.
  7. Lampit A, Suo C, Gates N, Kwok SSY, Naismith S et al. (2011). Temporal evolution of cognitive training-induced structural and functional brain plasticity. 10th National Emerging Researchers in Ageing Conference, University of New South Wales, Sydney., Accessed 23 May 2014.
  8. Gates NJ, Valenzuela M, Sachdev PS, Singh NA, Baune BT, et al. (2011) Study of Mental Activity and Regular Training (SMART) in at risk individuals: A randomised double blind, sham controlled, longitudinal trial. BMC Geriatrics, 11(19), doi: 10.1186/1471-2318-11-19.
  9. Erickson KI, Voss MW, Prakash RS, Basak C, Szabo A, et al. (2011). Exercise training increases size of hippocampus and improves memory. Proceedings of the National Academy of Sciences of the United States of America, 108(7), 3017-3022. doi: 10.1073/pnas.1015950108.
  10. Brookmeyer R, Johnson E, Ziegler-Graham K & Arrighi HM (2007). Forecasting the global burden of Alzheimer’s disease. Alzheimer’s & Dementia, 3(3), 186–191. doi: 10.1016/j.jalz.2007.04.381.

A new direction in HIV therapy

HIV is a worldwide problem – 35.3 million people are living with HIV or AIDS and 36 million people have died from AIDS related illnesses1. As the HIV/AIDS epidemic is such a big problem, there are many agencies working hard to come up with effective and efficient treatments. In a recent seminar at Macquarie University’s Australian School of Advanced Medicine, Professor Anthony Kelleher discussed the cutting edge HIV research his team has been conducting. His research at The Kirby Institute, University of NSW, focuses on how HIV reservoirs are established and maintained and how this information can help to develop a cure.

Currently, the only option for HIV treatment is the use of antiviral therapy. This treatment suppresses the replication of HIV virus particles by targeting different stages of the virus lifecycle, such as the entry of the virus particles into the cell, creation of DNA from virus RNA, insertion of the virus DNA into the cell’s nuclear DNA or preventing mature virus particles from leaving the cell (Figure 1)2.

Figure 1. Anti-viral drugs target different stages of the HIV lifecycle.

Figure 1. Anti-viral drugs target different stages of the HIV lifecycle.

Antiviral therapies work well, but they don’t eliminate the virus from the body3. As soon as patients stop anti-viral drug treatment, HIV levels can rapidly rise due to the stockpile of virus particles lurking in cells (the viral reservoir)4. This means patients with HIV need anti-viral drugs for the rest of their lives, otherwise the virus will return with vigor and the patient will relapse (Figure 2).

Figure 2. HIV+ patients currently take a cocktail of drugs to suppress the virus.

Figure 2. HIV+ patients currently take a cocktail of drugs to suppress the virus.

Staying on anti-viral drugs for a lifetime can have a lot of unwanted side effects, such as metabolic diseases and osteoporosis5. There are research teams developing a vaccine for HIV, but this is still in phase 1 of clinical trials (preliminary safety tests). A vaccine needs multiple rounds of trials and will take approximately 15 years before it can be used in the general population6.

Only one person has been cured of HIV – a patient with HIV developed an additional disease which required a bone marrow transplant. The bone marrow donor had a deletion of his CCR5 gene, a receptor for HIV. As the HIV receptor was no longer present the HIV could no longer bind and the patient was cured4. Unfortunately, a bone marrow transplant from a donor with a CCR5 gene deletion is not an option for everyone with HIV, so other avenues are being explored.

Professor Kelleher and his team are interested in developing alternatives to long-term medications and are looking at the genes of HIV and the immune system for a possible solution. The team has just recently received ethics clearance to start human clinical trials using siRNAs (small interfering RNAs) to degrade the CCR5 gene receptor for HIV. This method aims to stop expression of the HIV genes (silencing) which stops the virus particles from replicating7 (Figure 3). This will remove the viral reservoir, but the genes will still be present in the patient’s genome. This method has been effective for other viruses, such as the Human Papilloma Virus, Polio, Hepatitis B and Hepatitis C, and oncogenes have also been silenced using this method8,9.

The way retroviruses, such as HIV, replicate is by inserting their genetic material into the host cell’s genome and taking over the DNA replication machinery to produce messenger RNA and then proteins. The siRNAs can bind to the HIV messenger RNAs (Figure 3) and degrade them, stopping the creation of the proteins that create HIV particles10. Alternatively the siRNAs can bind to the DNA and change the chemical structure so the HIV genes can’t be transcribed4. The siRNAs are so specifically targeted to HIV strains that there is no chance of detrimental impacts on other genes10.

Figure 3. siRNAs degrade messenger RNA so it can’t be translated into protein (McManus & Sharp 2002).

Figure 3. siRNAs degrade messenger RNA so it can’t be translated into protein (McManus & Sharp 2002).

Another research group has shown that treatment with siRNAs works to silence an HIV-type virus in mice11 so the next step is to try this method with human HIV. Professor Kelleher’s team will start the treatment with a small group of HIV patients, following these steps:

  1. Identify HIV+ patients currently taking anti-viral drugs to suppress the virus;
  2. Treat with siRNA therapy;
  3. Stop anti-viral treatment; and
  4. Monitor the patients to see if the HIV stays suppressed.

If the HIV symptoms don’t return then the siRNAs have eliminated the viral reservoir and silenced the HIV. The siRNA treatment has been shown to be effective in human cells for up to 30 days in a laboratory setting. If the same is shown in human clinical trials, this could lead to a significant improvement for the quality of life for millions of HIV+ patients in the future.

Want to know more?

  1. World Health Organisation (2014.) HIV/AIDS,, accessed 22 May 2014.
  2. Mehellou Y & De Clercq E (2010). Twenty-Six Years of Anti-HIV Drug Discovery: Where Do We Stand and Where Do We Go? Journal of Medicinal Chemistry, 53(2), 521-538. doi: 10.1021/jm900492g.
  3. Suzuki K, Marks K, Symonds G, Cooper DA, Kelleher AD, et al. (2013). Promoter targeting shRNA suppresses HIV-1 infection in vivo through transcriptional gene silencing. Molecular Therapy – Nucleic Acids, 2, e137; doi: 10.1038/mtna.2013.64.
  4. Kent SJ, Reece JC, Petravic J, Martyushev A, Kramski M, et al. (2013). The search for an HIV cure: tackling latent infection. The Lancet, 13(7), 614-621. doi: 10.1016/S1473-3099(13)70043-4.
  5. Grund BA, Peng GA, Gibert CLB, Hoy JFC, Isaksson RLA, et al. (2009). Continuous antiretroviral therapy decreases bone mineral density. AIDS, 23(12), 1519-1529. doi: 10.1097/QAD.0b013e32832c1792.
  6. National Health and Medical Research Council, Commonwealth of Australia (2014). Australian Clinical Trials., accessed 22 May 2014.
  7. McManus MT and Sharp PA (2002). Gene silencing in mammals by small interfering RNAs. Nature Reviews Genetics, 3, 737-747. doi: 10.1038/nrg908.
  8. Saleh MC, Van Rij RP, Andino R (2004). RNA silencing in viral infections: insights from poliovirus. Virus Research, 102, 11–17. doi: 10.1016/j.virusres.2004.01.010.
  9. Li S-D, Chono S & Huang L (2008). Efficient Oncogene Silencing and Metastasis Inhibition via Systemic Delivery of siRNA. Molecular Therapy, 16(5), 942-946. doi: 10.1038/mt.2008.51.
  10. Suzuki, K, Ishida T, Yamagishi M, Ahlenstiel C, Swaminathan S, et al. (2011). Transcriptional gene silencing of HIV-1 through promoter targeted RNA is highly specific. RNA Biology, 8(6), 1035-1046. doi: 10.4161/rna.8.6.16264.
  11. Mitsuyasu RT, Merigan TC, Carr A, Zack JA, Winters MA, et al. (2009). Phase 2 gene therapy trial of an anti-HIV ribozyme in autologous CD34+ cells. Nature Medicine, 15, 285-292. doi: 10.1038/nm.1932.

iPhone remote medicine

The need for a bulky specialised piece of equipment and a trained operator limits medical diagnosis and subsequent treatment in remote and developing areas. Now a small lens can be attached to an iPhone to create a mobile microscope. No longer is the equipment or operator limiting as an image can be captured in the field and sent to a trained person for analysis.


Photo by Cindy Manly-Fields (Bioengineering Department, UC Berkeley)

Read more:
Mobile Microscopes by Jeff Akst – 1 June 2013