Synaesthesia : Training People to “See” Letters of the Alphabet as Colours

(University of Sussex) A new study has shown for the first time that people can be trained to “see” letters of the alphabet as colours in a way that simulates how those with synaesthesia experience their world.

The University of Sussex research, published today (18 November 2014) in  Scientific Reports, also found that the training might potentially boost IQ.

Synaesthesia is a fascinating though little-understood neurological condition in which some people (estimated at around 1 in 23) experience an overlap in their senses. They “see” letters as specific colours, or can “taste” words, or associate sounds with different colours.

A critical debate concerns whether the condition is embedded in our genes, or whether it emerges because of particular environmental influences, such as coloured-letter toys in infancy.

blocksWhile the two possibilities are not mutually exclusive, psychologists at the University’s Sackler Centre for Consciousness Science devised a nine-week training programme to see if adults without synaesthesia can develop the key hallmarks of the condition.

They found, in a sample study of 14, that not only were the participants able to develop strong letter-colour associations to pass all the standard tests for synaesthesia, most also experienced sensations such as letters seeming “coloured” or having individual personas (for instance, “x is boring”, “w is calm”).

One of the most surprising outcomes of the study was that those who underwent the training also saw their IQ jump by an average of 12 points, compared to a control group that didn’t undergo training.

Dr Daniel Bor, who co-led the study with Dr Nicolas Rothen, says: “The main implication of our study is that radically new ways of experiencing the world can be brought about simply through extensive perceptual training.

“The cognitive boost, although provisional, may eventually lead to clinical cognitive training tools to support mental function in vulnerable groups, such as Attention Deficit Hyperactivity (ADHD) children, or adults starting to suffer from dementia.”

Dr Rothen adds:

“It should be emphasised that we are not claiming to have trained non-synaesthetes to become genuine synaesthetes. When we retested our participants three months after training, they had largely lost the experience of ‘seeing’ colours when thinking about the letters. But it does show that synaesthesia is likely to have a major developmental component, starting for many people in childhood.”



Mind Before Matter: Do Negative Thoughts Increase Risk of Alzheimer’s Disease?

(Journal of Alzheimer’s Disease) Researchers from the Institute of Psychiatry, Psychology & Neuroscience (IoPPN) at King’s College London have proposed that repetitive negative thinking (RNT), a common symptom of many psychological disorders, may increase the risk of developing Alzheimer’s disease.

Until recently, research into Alzheimer’s disease has focused on how physical factors are linked to the onset of symptoms. However, scientists at the IoPPN suggest that there are psychological factors that make a person more vulnerable to Alzheimer’s disease; and that these factors occur before any physical indicators of the disease emerge.

In an article published in the Journal of Alzheimer’s Disease, the researchers argue that a habit of negative thinking over a prolonged period of time (RNT) can have a harmful effect on the brain’s capacity to think, reason and form memories. RNT is a common behaviour in people suffering from depression, anxiety, sleep disorders, post-traumatic stress disorder, and life stress; which are themselves associated with increased risk of Alzheimer’s.

RNT can occur without us being consciously aware of it and consumes our finite capacity of brain resources. Importantly, RNT also triggers a physical stress response in the brain, which over a prolonged period of time may cause damage and reduce the brain’s resilience to Alzheimer’s disease.

Genetics has been shown to play a role in Alzheimer’s disease and people with a particular variant of a gene known as APOE e4 have increased risk of Alzheimer’s. However, not everyone who has this gene variant will get Alzheimer’s, which suggests that other influences may be involved. Previous research has shown that people who possess this gene variant and who suffer from psychological disorders such as depression are at an even higher risk of developing Alzheimer’s.

Robert Howard, Professor of Old Age Psychiatry and Psychopathology at the IoPPN, says:

“Treatments that reduce RNT exist, and we believe that they may reduce the risk of Alzheimer’s disease. Further research is needed to verify this concept however our new proposal offers a promising line of scientific investigation to reduce the heavy societal burden posed by Alzheimer’s disease.”

Dr Natalie Marchant, Lecturer in Old Age Psychiatry at the IoPPN, King’s College London, says:

“We propose that the way that we think may impact our risk for developing Alzheimer’s disease. If future research supports this hypothesis this would have implications for the treatment of the disease through psychological interventions.”



Spice Up Your Memory with Tumeric

(Monash University) Adding just one gram of turmeric to breakfast could help improve the memory of people who are in the very early stages of diabetes and at risk of cognitive impairment.

The finding has particular significance given that the world’s ageing population means a rising incidence of conditions that predispose people to diabetes, which in turn is connected to dementia.


Early intervention could help to reduce the burden, whether by halting the disease or reducing its impact, said Emeritus Professor Mark Wahlqvist, from the Monash Asia Institute at Monash University.

Professor Wahlqvist recently led a study in Taiwan that tested the working memory of men and women aged 60 or older who had recently been diagnosed with untreated pre-diabetes.

“Working memory is widely thought to be one of the most important mental faculties, critical for cognitive abilities such as planning, problem solving and reasoning,” he said.

“Assessment of working memory is simple and convenient, but it is also very useful in the appraisal of cognition and in predicting future impairment and dementia.”

In the placebo-controlled study, subjects were given one gram of turmeric with an otherwise nutritionally bland breakfast of white bread. Their working memory was tested before and some hours after the meal.

“We found that this modest addition to breakfast improved working memory over six hours in older people with pre-diabetes,” Professor Wahlqvist said.

Turmeric is widely used in cooking, particularly in Asia. Its characteristic yellow colour is due to curcumin, which accounts for 3 to 6 per cent of turmeric and has been shown by experimental studies to reduce the risk of dementia.

“Our findings with turmeric are consistent with these observations, insofar as they appear to influence cognitive function where there is disordered energy metabolism and insulin resistance,” Professor Wahlqvist said.

The study, which was published in the Asia Pacific Journal of Clinical Nutrition, also involved a number of research institutes in Taiwan.



Danger of Repeat Head Injuries: Brain’s Inability to Tap Energy Source

(The Ohio State University) Two or more serious hits to the head within days of each other can interfere with the brain’s ability to use sugar – its primary energy source – to repair cells damaged by the injuries, new research suggests.

The brain’s ability to use energy is critical after an injury. In animal studies, Ohio State University scientists have shown that brain cells ramp up their energy use six days after a concussion to recover from the damage. If a second injury occurs before that surge of energy use starts, the brain loses its best chance to recover.

In mice, the lack of energy use for recovery led to inflammation, degeneration of brain cell segments and problems with learning and memory.

In new work presented Sunday (11/16) at Neuroscience 2014, the annual meeting of the Society for Neuroscience, these same scientists have observed that even if the required glucose is present in the brain, faulty insulin signals in an injured brain don’t allow cells to take up the sugar and use it.

All clinical signs suggest that two head injuries close together are dangerous and can even be deadly. But the science behind what’s actually going on in the brain is still unclear – and knowing these details could help in deciding when to return athletes to play or military members to service, said lead author Zachary Weil, assistant professor of neuroscience at Ohio State.

“Lots of data show that if two head injuries occur close together, it’s not like 1 plus 1. It’s more like 1 plus 10,” Weil said. “So our goals are to understand what it is about injuries close together that makes us more vulnerable, and can we eventually use some sort of biological signal to tell when it’s safe to go back?”

Weil said the discovery that insulin resistance plays a role in brain recovery after injury could also help explain the development of a brain disease seen in professional athletes who have had multiple traumas to the head – chronic traumatic encephalopathy, or CTE. Several CTE symptoms resemble Alzheimer’s disease – memory problems, disorientation and trouble concentrating – and the link between defective insulin signals and Alzheimer’s is already established.

“With injury, the damaged cells are not able to use energy even though they need it and the glucose is there. It appears that’s because the signals are messed up,” he said. “It’s the same thing seen in Alzheimer’s patients. Cells are chronically undernourished even though the sugar level might be high.”

In earlier animal studies, Weil and colleagues compared the effects of head injuries that occurred either three days or 20 days apart. Of all the animals, the mice injured three days apart had higher inflammation in the brain, more degeneration of axons – the long, slender extension of the nerve cell body – and problems learning how to navigate a maze and remembering the lessons they did manage to learn. Neurons need healthy axons to communicate with each other.

Mice with a single injury or head blows 20 days apart both showed the surge in brain energy use six days after the injury. The brains in mice injured three days apart never developed such a high level of glucose use.

“With the second injury, demands for energy might outstrip the ability of the damaged cells to actually use the energy,” Weil said.

This research was published in a recent issue of the journal Neurobiology of Disease.

In follow-up work presented at Neuroscience 2014, the researchers examined brain tissue in mice that had experienced no injury, one concussion or two head injuries 24 hours apart. After treating the tissue with insulin, the scientists measured activation levels of a key protein in the insulin signaling process.

In mice with no injury, the protein activation was increased by the presence of insulin. But the injured brains did not respond to the presence of insulin at all. Without activation of those signals, brain cells have no way to make use of their glucose energy source.

“This means that traumatic brain injury induces insulin resistance in the brain,” Weil said. “So we need to work on finding ways to acutely increase insulin sensitivity rather than increasing the actual amount of insulin in the brain.”

Weil conducted the research with co-authors Kristopher Gaier and Kate Karelina, both of Ohio State’s Department of Neuroscience.

Scientific Presentation: 8:15 to 8:30 a.m. Nov. 16, Washington Convention Center Room 150B, Symposium 113.02, “Brain: Cellular and molecular mechanisms” 



Alzheimer’s Disease Treatment: Positive Phase 1 Data for ANAVEX 2-73 Drug Candidate

( Anavex Life Sciences Corp) Data Presented at CNS Summit 2014 Supports Commencement of Phase 2 Clinical Trial in Alzheimer’s Patients

Anavex announced full data results from the Phase 1 clinical trial of ANAVEX 2-73, the Company’s lead investigational oral treatment for Alzheimer’s, which has shown potential in preclinical studies to prevent, halt and/or reverse the course of the disease.

Observed adverse events included moderate and reversible headache and dizziness, which is common in drugs that target central nervous system (CNS) conditions, including Alzheimer’s.

No serious side effects were reported in this randomized, double-blind, placebo-controlled study, there was no study discontinuation due to adverse events, ANAVEX 2-73 was found to be safe and well tolerated, and the results indicate a favorable pharmacokinetics profile. Findings from the Phase 1 clinical trial were presented at CNS Summit 2014 in Boca Raton, Florida.

A Phase 2a clinical trial of ANAVEX 2-73 and ANAVEX PLUS, the combination of ANAVEX 2-73 and donepezil (Aricept®), is now underway.

“We are extremely encouraged by the strong safety profile of ANAVEX 2-73 as evidenced by the Phase 1 trial data. Treatment of Alzheimer’s disease generally requires ongoing drug administration, which underscores the importance for any potential new drug to have a low side effect profile,” said Christopher U. Missling, PhD, President and Chief Executive Officer of Anavex.

“Following recent regulatory approval to start a Phase 2a efficacy study of ANAVEX 2-73 in Alzheimer’s patients, we are excited to advance our investigational compound as a potential treatment option for this devastating disease with high unmet medical needs.”

The Phase 1 clinical trial was a randomized, double-blind, placebo-controlled study in 22 healthy male volunteers. The participants received single, ascending oral doses of ANAVEX 2-73 ranging from 1 mg to 60 mg. The primary objective of the trial was to evaluate safety and tolerability together with pharmacokinetic parameters.

  • Safety: No serious side effects were reported. There was no study discontinuation due to adverse events. No dose-limiting adverse events or lab abnormalities at doses of 1, 10, 30, 40 and 50mg were observed.
  • Tolerability: Maximum tolerated dose (MTD) of ANAVEX 2-73 was defined as 55mg. Observed adverse events at doses above the MTD included dizziness and headache, which were moderate in severity and reversible. These side effects are often seen with drugs that target CNS conditions, including Alzheimer’s disease. Across all doses, there were no differences in blood pressure and resting heart rate. Analysis of electrocardiograms (ECG) did not reveal any dose-related or time-dependent changes and the QT interval did not reveal any clinically significant changes. Additionally, no sign could be detected for any dose- or time-dependent changes for any of the hematology, biochemistry, and coagulation parameters.
  • Pharmacokinetics (PK): ANAVEX 2-73 was determined to be suitable for daily oral dosing based on its PK profile. PK data revealed biotransformation of ANAVEX 2-73 to its main metabolite, which also actively targets sigma-1 and muscarinic receptors like its parent drug ANAVEX 2-73. Both maximum plasma concentration (Cmax), which relates to absorption and distribution of the drug in the blood, and area under the plasma concentration-time curve (AUC), which represents the total drug exposure over time, showed dose-proportional linear increases for both ANAVEX 2-73 and its metabolite. The biological half-life (T1/2) for ANAVEX 2-73 was 8.56 hours and 28.74 hours for its metabolite.

The poster entitled “A Phase 1 Dose Escalation Study to Investigate Safety, Tolerability, and Pharmacokinetics of ANAVEX 2-73 in Healthy Male Subjects” was co-authored by Ole Voges and Ingo Weigmann both of ABX-CRO, Norman Bitterlich of Medizin & Service GmbH, Christoph Schindler of Clinical Research Center, and Christopher U. Missling, President and CEO of Anavex.


ANAVEX 2-73 is an orally available small molecule being investigated for the treatment of Alzheimer’s disease. In addition to preclinical data indicating that ANAVEX 2-73 has the potential to prevent, halt and/or reverse the course of Alzheimer’s disease, there was a highly encouraging synergistic effect observed between ANAVEX 2-73 and donepezil (Aricept®). The combined therapeutic, called ANAVEX PLUS, produced up to 80% greater reversal of memory loss in Alzheimer’s disease models versus when the drugs were used individually.

About Alzheimer’s Disease

Today, Alzheimer’s disease remains the largest unmet medical need in neurology. More than 25 million people are currently diagnosed with Alzheimer’s, with the associated cost of care estimated to exceed $200 billion annually. By 2050, the disease is expected to afflict 100 million. Alzheimer’s disease is a neurological disorder generally characterized by memory loss and cognitive decline. A neurodegenerative form of dementia, the disease begins with mild symptoms and becomes progressively worse.

About Anavex Life Sciences Corp

Anavex Life Sciences Corp. (OTCQB: AVXL) is a publicly traded biopharmaceutical company dedicated to the development of novel drug candidates to treat Alzheimer’s disease, other Central Nervous System (CNS) diseases, and various types of cancer. Anavex’s lead drug candidates, ANAVEX 2-73 and ANAVEX PLUS, the combination of ANAVEX 2-73 and donepezil (Aricept®), are currently in a Phase 2a clinical trial for Alzheimer’s disease. ANAVEX 2-73 is an orally available drug candidate that targets sigma-1 and muscarinic receptors and successfully completed Phase 1 with a clean data profile. Preclinical studies demonstrated its potential to halt and/or reverse the course of Alzheimer’s disease. The drug combination ANAVEX PLUS produced up to 80% greater reversal of memory loss in Alzheimer’s disease models versus when the drugs were used individually. Further information is available at


Coping Strategies Therapy Significantly Improves Dementia Carers’ Mental Health and Quality of Life

(MedicalXpress) A brief coping strategies therapy which provides stress relief and emotional support for people caring for relatives with dementia can reduce depression and anxiety and improve wellbeing at no extra cost to standard care, new research published in The Lancet Psychiatry suggests.

The study led by Gill Livingston, Professor of Psychiatry of Older People at University College London in the UK, found that receiving the START (STrAtegies for RelaTives) programme were seven times less likely to develop clinically significant depression than those given usual care, with benefits lasting for at least 2 years.

Two-thirds of people with live at home, with their family providing most of their care. There are around 670 000 of these in the UK and more than 15 million in the USA. However, about 40% of family carers develop clinical depression or anxiety, which typically leads to care breakdown, and results in individuals with dementia moving to a care home.

Livingston and colleagues randomly assigned 260 family carers who were free from depression at the start of the study to either the 8-session START programme (173 carers) or to usual care consisting of medical, psychological, and social services for the person with dementia (control; 87). START was delivered by non-clinically trained psychology graduates working on a one-to-one basis with family carers at their home to identify individual difficulties and implement coping strategies (eg, help with accessing and relaxation).

Assessments were made of depression and anxiety using the Hospital Anxiety and Depression Scale (HADS) and of cost-effectiveness over 2 years.

On average, carers in the START group reported a significant (2.58 point) improvement in HADS total score compared to the usual care group in both the short (8 months) and long term (24 months). Moreover, START was no more expensive than usual care, and showed the best value for money based on NICE cost effectiveness thresholds.

According to Professor Livingston,

“Worldwide, there are an estimated 44 million people with dementia, and this figure is likely to double every 20 years. Too often people forget the substantial effect dementia has on family members caring for with dementia. Policy frameworks assume that families will remain the main providers of their (unpaid) support. This new cost-neutral programme is an effective way to support carers and improve their mental health and quality of life and should be made widely available.”

Writing in a linked Comment, Sube Banerjee, Professor of Dementia at the University of Sussex, Brighton, UK, says,

“the START intervention should be offered as individual therapy to all family carers of people with dementia as part of the support with a timely diagnosis. START should be a specified component of the diagnostic services for dementia (such as memory services) that are commissioned by Clinical Commissioning Groups throughout the UK.”



Trans Fat Consumption is Linked to Diminished Memory in Working-aged Adults

(American Heart Association) High trans fat consumption is linked to worse memory among working-age men, according to research presented at the American Heart Association’s Scientific Sessions 2014.

In a recent study of approximately 1,000 healthy men, those who consumed the most trans fats showed notably worse performance on a word memory test. The strength of the association remained even after taking into consideration things like age, education, ethnicity and depression.

 “Trans fats were most strongly linked to worse memory, in young and middle-aged men, during their working and career-building years,” said Beatrice A. Golomb, M.D., Ph.D., lead author and professor of medicine at the University of California-San Diego.

“From a health standpoint, trans fat consumption has been linked to higher body weight, more aggression and heart disease. As I tell patients, while trans fats increase the shelf life of foods, they reduce the shelf life of people.”

Golomb and her coauthor studied adults who had not been diagnosed with heart disease, including men age 20 or older and postmenopausal women. Participants completed a dietary questionnaire, from which the researchers estimated participants’ trans fat consumption. To assess memory, researchers presented participants with a series of 104 cards showing words. Participants had to state whether each word was new or a word duplicated from a prior card.

They found:

  • Among men under age 45, those who ate more trans fats showed notably worse performance on the word memory test. The strength of the association remained even after taking into consideration things like age, education, ethnicity and depression.
  • Each additional gram a day of trans fats consumed was associated with an estimated 0.76 fewer words correctly recalled.
  • For those eating the highest amounts of trans fats, this translated to an estimated 11 fewer words (a more than 10 percent reduction in words remembered), compared to adults who ate the least trans fat. (The average number of words correctly recalled was 86.)

“Foods have different effects on oxidative stress and cell energy,” Golomb said. In a previous study, we found chocolate, which is rich in antioxidants and positively impacts cell energy, is linked to better word memory in young to middle-aged adults. In this study, we looked at whether trans fats, which are prooxidant and linked adversely to cell energy, might show the opposite effect. And they did.”

Oxidative stress is associated with the development of diseases such as heart disease and cancer.

Industrial trans fats are artificially produced to turn liquid oils into solids at room temperature and extend food shelf life. They can be found in margarines, fast foods, baked goods, snack foods, frozen pizza, coffee creamers and some refrigerated doughs.  The Food and Drug Administration is taking further steps to reduce the amount of artificial trans fats in the U.S. food supply.

Analyses in younger women are needed to determine whether effects extend to this group, Golomb said.

The co-author is Alexis K. Bui, B.S.  Author disclosures are on the manuscript.

The National Heart, Lung, and Blood Institute supported the study.

Additional Resources:


Statements and conclusions of study authors that are presented at American Heart Association scientific meetings are solely those of the study authors and do not necessarily reflect association policy or position. The association makes no representation or warranty as to their accuracy or reliability. The association receives funding primarily from individuals; foundations and corporations (including pharmaceutical, device manufacturers and other companies) also make donations and fund specific association programs and events. The association has strict policies to prevent these relationships from influencing the science content. Revenues from pharmaceutical and device corporations are available at

Note: Actual presentation is 3 p.m. CT /4  p.m. ET, Tuesday, Nov. 18, 2014 (South Hall A2, Core 2).



Total Recall: Study Identifies New Player in Brain Function and Memory

(McGill University Health Center) Is it possible to change the amount of information the brain can store? Maybe, according to a new international study led by the Research Institute of the McGill University Health Centre (RI-MUHC).

The research has identified a molecule that puts the brakes on brain processing and when removed, brain function and memory recall is improved. Published in the latest issue of Cell Reports, the study has implications for neurodevelopmental and neurodegenerative diseases, such as autism spectral disorders and Alzheimer’s disease.

“Previous research has shown that production of new molecules is necessary for storing memories in the brain; if you block the production of these molecules, new memory formation does not take place,” says RI-MUHC neuroscientist, Dr. Keith Murai, the study’s senior author and Associate Professor in the Department of Neurology and Neurosurgery at McGill.

“Our findings show that the brain has a key protein that limits the production of molecules necessary for memory formation. When this brake-protein is suppressed, the brain is able to store more information.

FXR1P: a controller of certain forms of memory

Dr. Murai and his colleagues used a mouse model to study how changes in brain cell connections produce new memories. They demonstrated that a protein, FXR1P (Fragile X Related Protein 1), was responsible for suppressing the production of molecules required for building new memories. When FXR1P was selectively removed from certain parts of the brain, these new molecules were produced that strengthened connections between brain cells and this correlated with improved memory and recall in the mice.

Disease link

“The role of FXR1P was a surprising result,” says Dr. Murai. “Previous to our work, no-one had identified a role for this regulator in the brain. Our findings have provided fundamental knowledge about how the brain processes information. We’ve identified a new pathway that directly regulates how information is handled and this could have relevance for understanding and treating brain diseases.”

“Future research in this area could be very interesting,” he adds. “If we can identify compounds that control the braking potential of FXR1P, we may be able to alter the amount of brain activity or plasticity.

For example, in autism, one may want to decrease certain brain activity and in Alzheimer’s disease, we may want to enhance the activity. By manipulating FXR1P, we may eventually be able to adjust memory formation and retrieval, thus improving the quality of life of people suffering from brain diseases.”

About the study

This research was made possible with funding from the Canadian Institutes of Health Research (CIHR), the Natural Sciences and Engineering Research Council of Canada, and National Institutes of Health (U.S.A.).