A new treatment for heart attack will soon be available for emergency teams and the emergency ambulance service (SAMU)

A new strategy for emergency anticoagulant treatment for patients with acute myocardial infarction has been put in place by a team led by Philippe-Gabriel Steg at Inserm Unit 698 (Haemostasis, Bioengineering, Immunopathology and Cardiovascular Remodelling), at Hôpital Bichat, AP-HP, Université Paris Diderot). These results from the EUROMAX clinical trial are published in The New England Journal of Medicine.

Myocardial infarction, commonly called “heart attack,” remains the leading cause of death worldwide, and affects nearly 100,000 individuals a year in France. The reference treatment is urgent dilation of the arteries to enable the blood to circulate to the heart (This medical procedure is known as primary angioplasty). Angioplasty requires injectable anticoagulant treatment for which several options are available.


An international team led by Philippe-Gabriel Steg at Inserm Unit 698 (Haemostasis, Bioengineering, Immunopathology and Cardiovascular Remodelling), at Hôpital Bichat, AP-HP, Université Paris Diderot) has just reported the results of a large international clinical trial carried out in 9 European countries, on nearly 2,200 patients, testing the administration of anticoagulant treatment prior to arrival in hospital by emergency teams and the emergency ambulance service, and comparing the two strategies, in The New England Journal of Medicine . The first is based on heparin (traditional treatment), the other on a more specific anticoagulant, bivalirudin. One of the main drawbacks of these anticoagulant treatments is the risk of associated haemorrhage. “By dilating the arteries, we also thin the blood, with the risk of uncontrolled bleeding if haemorrhage occurs,” explains Philippe-Gabriel Steg.

After 30 days of monitoring, bivalirudin reduced the risk of death or serious bleeding by 8.5 to 5.1% and the risk of death, myocardial infarction or major bleed by 9.2 to 6.6%, compared with the strategy using heparin.

This benefit was mainly linked to the reduction in serious bleeding, at the cost of an increased risk of stent thrombosis . “The benefits are robust and consistent for all sub-groups tested, and in particular, consistent regardless of the type of oral anti-clotting treatment or route of arterial access used for angioplasty (via the radial or femoral artery),” explains Philippe-Gabriel Steg.
These results open up the way to using bivalirudin as an anticoagulant at the pre-hospital phase of myocardial infarction in patients being urgently transferred. They represent progress in the treatment of myocardial infarction that can be immediately used.
The EUROMAX trial was conducted with the support of The Medicines Company. It is registered in Clinical, under the reference NCT01087723.

Physical exercise to prevent the consequences of falls in older people

Well-designed physical exercise programmes may limit the risk of injury from falls in older people. According to an article published today by a team led by Patricia Dargent, Research Director at Inserm Unit 1018 (Centre for Research in Epidemiology and Population Health), not only can such exercise reduce the incidence of falls, it can also reduce their severity. For example, these programmes help to avoid hip fractures (neck of the femur), which require medical attention and lead to a loss of autonomy that is sometimes considerable in older people. 

These results, obtained from a survey of the literature, have been published in The British Medical journal.

Exercice personnes âgées


From a certain age, some activities that had seemed routine can easily cause an accident (slipping on a carpet, climbing a step-ladder to replace a light-bulb, etc.) Moreover, whereas a fall may be of no great consequence for a healthy individual (who gets away with a hefty bruise), it can turn out to be serious and disabling for an older person. These injuries are very common, and constitute a major cause of long-term pain and a reduction in the ability to function. They also increase the risk of loss of autonomy and the need for nursing-home care, which constitutes a high economic cost.

Although the effect of exercise on the prevention of falls had already been demonstrated, its impact on the incidence of serious injury had not been considered. The latter was analysed by the researchers at Inserm, who reviewed all existing programmes to see if they were associated with a significantly lower risk of fractures or other serious injuries.

Their study included 17 studies carried out all over the world, involving 2,195 participants who exercised, and 2,110 who did not (control groups). The mean age of participants in these programmes was 76 years, and 77% of these participants were women.

Among the programmes reviewed, two consisted of doing tai-chi, whereas the others consisted of doing simple balance training exercises, most often combined with exercise to strengthen the muscles.

Results of the meta-analysis suggest that this type of programme helps to significantly reduce the incidence of falls leading to serious trauma, fracture, and/or requiring medical attention.

This study, the first of its kind, suggests that reducing the risk of falling, and improving the protective reflexes during a fall (such as putting out one’s hands to save oneself) by doing regular specific exercises might be a simple and feasible way to prevent fractures and other serious injuries in older people. The researchers see this as “additional evidence encouraging patients to participate in exercise programmes for falls prevention.”

Further investigation

Patricia Dargent’s team is currently conducting a research programme known as “Ossébo.” This is a randomised controlled study of physical exercise in the maintenance of balance and prevention of falls and fractures, and is being carried out on women aged 75 and over, living in their own homes. The initial results of this programme should be published in 2014.

Major advance in understanding Alzheimer’s disease: 11 new genetic susceptibility factors discovered

The largest international study ever conducted on Alzheimer’s disease, as part of the IGAP (International Genomics of Alzheimer Project) international consortium, coordinated by the joint research unit comprising Inserm, the Pasteur Institute at Lille-University Lille Nord de France ‘Public health and molecular epidemiology of diseases associated with ageing’ and LabEx DISTALZ, directed by Philippe Amouyel, has identified eleven new regions of the genome involved in the appearance of this neuro-degenerative disease. This work provides an overview of the molecular mechanisms at the root of the disease, revealing a better understanding of the physiopathology of this curse. These results, described in an article published in the journal Nature Genetics dated 27 October 2013, were obtained through a unique global collaborative effort by the best researchers in the field.

Since 2009, 10 genes linked to Alzheimer’s disease have been discovered, providing a better understanding of this dreadful illness. However, a large part of individual susceptibility to develop this disease still remains unknown. Characterising this individual susceptibility carried by our genome required being able to compare patients’ DNA with that from healthy people, to find a few hundred variations among more than 3.5 billion genes making up our genome. Such an approach meant analysing the genomes of thousands of individuals, which cannot be done at a team scale or even that of a single country.

For this reason, in February 2010, managers from the four largest international research consortia on the genetics of Alzheimer’s disease decide to join forces to accelerate the discovery of new genes. In less than 3 years, under the IGAP programme, researchers have succeeded in identifying more genes than over the previous 20 years. They set up their study in two phases. The first consisted of reanalysing all their existing data based on common criteria, a total of more than 17,000 cases of Alzheimer’s disease collected in Europe and North America, comparing them to some 37,000 non-diseased controls. Using advances in human genome sequencing (1000 Genomes project), they were able to compare the distribution of more than 7 million mutations between these cases and controls, so as to select only 11,632 of them from this first phase.

In the second phase, researchers verified these results in independent samples from 11 different countries, totalling 8,572 patients and 11,312 controls. This confirmed the discovery of 11 new genes in addition to those already known and to locate 13 others still being confirmed.

These 11 new genes offer new opportunities for understanding the appearance of Alzheimer’s disease. One of the most significant associations has been found in the HLA-DRB5/DRB1 region of the major histocompatibility complex. This discovery is interesting for more than one reason. Firstly, it confirms the immune system’s involvement in the disease. In addition, this same regions is also found associated with two other neuro-degenerative diseases, multiple sclerosis and Parkinson’s disease. Another link could also be made with the SLC24A4 locus, which codes a protein involved in development of the iris and in the colour variation of hair and skin, and which is associated with the risk of high blood pressure.

Some of these new genes confirm known hypotheses about Alzheimer’s disease, particularly the role of the amyloid pathway (SORL1, CASS4) and the Tau protein (CASS4, FERMT2). The role of the immune response and inflammation (HLA-DRB5/DRB1, INPP5D, MEF2C), already implicated by previous work from Inserm unit 744 (CR1[i], TREM2[ii]), is strengthened, as well as the role of cellular migration (PTK2B), lipid transport and endocytosis (SORL1). New hypotheses have also appeared, associated with hippocampal synaptic function (MEF2C, PTK2B), the cytoskeleton and axonal transport (CELF1, NME8, CASS4), as well as myeloid and microglial cell functions (INPP5D).

For the researchers, this discovery results in three main consequences. Firstly, this observation provides a better understanding of the physiopathology of Alzheimer’s disease, an essential step to discovering new treatments. Furthermore, this genome analysis better identifies the genetic profile of patients with a risk of developing Alzheimer’s disease. Finally, this work demonstrates that, faced with the complexity of such a disease, only the combined strength of global research will allow solutions to be found more quickly for this 21st century curse.

About Alzheimer Disease

These results, which demonstrate the many advances in understanding Alzheimer’s disease, involved teams from LabEx Distalz, and were able to be obtained through the support of the National foundation for Scientific Cooperation on Alzheimer’s disease and similar diseases, as well as the genotyping and analytical capabilities of the CEA National Genotyping Centre, the Study Centre for Human Polymorphism and the Pasteur Institute at Lille.

With the increasing life expectancy of human populations, the number of patients affected by Alzheimer’s disease is tending to rise in France and throughout the world. The leading cause of disorders of the memory and intellectual functions in the elderly, this illness is therefore a major challenge for public health.

Alzheimer’s disease is one of the main causes of dependency in the elderly. It results in a deterioration of neurons in different regions of the brain. It is manifested by growing alteration in memory and cognitive functions, as well as by behavioural problems leading to progressive loss of independence. In France, Alzheimer’s disease affects more than 850,000 people and represents a major social and economic cost.

Alzheimer’s disease is characterised by development of two types of brain lesions: amyloid plaques and neurofibrillary degeneration. Amyloid plaques arise from extracellular accumulation of a peptide, the amyloid β peptide (Aβ), in specific areas of the brain. Neurofibrillary degeneration is intra-neural lesions arising from abnormal aggregation, in the form of filaments, of a protein called the Tau protein.

Identifying genes that contribute to the appearance of Alzheimer’s disease and its development will lead more rapidly to tackling the physiopathological mechanisms underlying this disease, to identifying target proteins and metabolic pathways for new treatments, and to offering methods to identify subjects at greatest risk when effective preventive treatments are available.

The International Genomics of Alzheimer Project, IGAP

In February 2011, researchers from the four leading research consortia into the genetics of Alzheimer’s disease were brought together to speed up the discovery and mapping of genes involved in Alzheimer’s disease. Their research work was conducted in European and North American universities. They combined the knowledge, staff and resources of the European Alzheimer’s Disease Initiative (EADI) in France, directed by Philippe Amouyel, doctor and researcher, Director of the joint research unit comprising Inserm, the Pasteur Institute at Lille-University Lille 2 ‘Public health and molecular epidemiology of diseases associated with ageing’ and LabEx DISTALZ. The Alzheimer’s Disease Genetics Consortium (ADGC) in the United States, directed by Gerard Schellenberg, researcher at the Pennsylvania University Faculty of Medicine. The Genetic and Environmental Risk in Alzheimer’s Disease (GERAD) in the United Kingdom, directed by Julie Williams, researcher at Cardiff University. Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE), directed by Sudha Seshadri, doctor at Boston University.


[i] Genome-wide association study identifies variants at CLU and CR1 associated with Alzheimer’s disease.

Lambert JC et al. Nature Genetics 2009. 41: 1094-1099.

[ii] TREM2 variants in Alzheimer’s disease.

Guerreiro R, et al. N Engl J Med. 2013; 368(2): 117-27.

Obesity: a new appetite-increasing mechanism discovered

Despite their efforts, many morbidly obese people continue to consume too much food (hyperphagia) compared to their reserves and their needs. And yet, the hunger hormone, called ghrelin, is most frequently found at a normal or even lower level in these patients. The Inserm Unit 1073 team “Nutrition, inflammation and dysfunction of the gut-brain axis” (Inserm/University of Rouen) has just explained this mechanism causing this paradoxical hyperphagia. Certain antibodies have a greater affinity for ghrelin in obese patients, leading to extended appetite stimulation.

These results are published in the journal Nature Communications, on 25 October 2013.

Obesity affects more than 15% of adults in France, and its constitutive mechanisms are still not completely explained. Normally, fine control of weight and food intake is coordinated by a specialised part of the brain (the hypothalamus). It adjusts food intake depending on reserves and needs. In this way, after a period of excessive food intake and weight gain, a healthy subject will tend spontaneously to reduce their food intake for a while to return to their previous weight.

In many of the morbidly obese, this mechanism is faulty: despite their efforts, they continue to consume too much food (hyperphagia), contributing to maintaining a higher weight or even increasing it further. Even so, their brain should take in the information about over-eating and reduce food intake to encourage weight loss. This observation is all the more surprising given that the hunger hormone ghrelin, produced by the stomach and acting on the hypothalamus, is most frequently found at a normal, or even a reduced level in obese patients.

The study conducted by Sergueï Fetissov and the team from joint research unit 1073 “Nutrition, inflammation and dysfunction of the gut-brain axis” (Inserm/University of Rouen), directed by Pierre Déchelotte, collaborating with Prof Akio Inui’s team at the University of Kagoshima (Japan), reveals the molecular mechanism of this paradoxical hyperphagia.

The researchers have highlighted the presence of specific antibodies, or immunoglobulins, in the blood of obese patients, antibodies that recognise ghrelin and regulate appetite.

By binding to ghrelin, the immunoglobulins protect the hunger hormone from being broken down rapidly in the bloodstream. The ghrelin can then act on the brain for longer and stimulate appetite.


Section of rat stomach showing ghrelin-producing cells (in red) and immune cells (in green). © Inserm / S. Fetissov

“The immunoglobulins have different properties in obese patients“, explains Sergueï Fetissov, researcher in the Inserm unit in Rouen and main author of the study. “They are more strongly ‘attracted’ to ghrelin than in subjects of normal weight or in anorexic patients. It is this difference in ‘affinity’ that enables the immunoglobulins to transport more ghrelin to the brain and boost its stimulating action on food intake“, he continues.

The research team has confirmed this mechanism by experiments in rodents. When ghrelin was administered in combination with immunoglobulins extracted from the blood of obese patients, or with immunoglobulins derived from genetically-obese mice, they stimulated food intake more strongly. Conversely, when ghrelin only was given, or combined with immunoglobulins from non-obese people or mice, the rodents were better able to regulate their appetite by restricting food intake.

“Our discover open a new opportunity to design treatments acting on the basis of this mechanism to reduce hyperphagia observed in cases of obesity“, emphasises Pierre Déchelotte, Director of the joint Inserm/University of Rouen unit.

This study extends other work by the research team, published in 2011, on the role of immunoglobulins interfering with different hormones acting on appetite, satiety or anxiety in cases of anorexia, bulimia or depression, and on the probable involvement of intestinal flora (microbiotic) in these interactions.

“Our results could also be used to study the opposite phenomenon, loss of appetite, such as observed in cases of anorexia“, concludes Pierre Déchelotte.

Memory brain systems help resisting temptations

Memory brain systems help resisting temptations – found a recent study led by researchers of the Brain & Spine Institute in Paris. How can some people resist the attraction of immediate pleasures and pursue long-term goals, while others easily succumb and compromise their ultimate expectations? One secret factor might lie in the activity of a deep brain structure: the hippocampus.

Geschäftsmann, Erfolg, Geschäftsidee, Icons


© Fotolia

Economists have been interested for decades in the conflict between smaller-sooner and larger-later rewards. Understanding how humans make inter-temporal choices, such as drinking tonight versus good health later, is crucial for designing insurance policy or anti-alcohol campaigns. This issue has recently been taken to brain scanners, in which volunteers were asked to make choices between monetary payoffs, for instance $10 now versus $11 tomorrow. Using this type of paradigm, scientists found that the dorsolateral part of the prefrontal cortex, a region known to implement behavioral control, was crucial for making patient choices – waiting for higher but delayed payoffs.

However, these paradigms miss an essential feature of the inter-temporal conflicts we have to face in everyday life, says study leader Mathias Pessiglione: immediate rewards can be perceived through our senses, whereas future rewards must be represented in our imagination. To reproduce this situation in the lab, the authors used more natural rewards like food items (for instance, a beer today or a bottle of champagne in a week for now). Volunteers were confronted to choices between immediate rewards presented as pictures, and future rewards presented as texts. In this case specifically, the ability to select future rewards was linked to the amount of hippocampus activity. To complete the demonstration, patients with hippocampus damage due to Alzheimer’s disease were tested in the same choice task. Contrary to patients with prefrontal degeneration, who exhibited excessive impulsivity in all sorts of choices, Alzheimer’s patients were specifically biased towards immediate rewards when future rewards had to be imagined.

This is because the hippocampus is necessary for imagining future situations with a richness of details that make them attractive enough – says Dr Pessiglione. Indeed, this structure has long been considered as essential for storing past episodes, but scientists have recently discovered that it is also involved in simulating future situations. The consequence is that patients with hippocampus damage suffer not only from memory deficits but also from a difficulty in imagining goals that would counter the attraction of immediate rewards and motivate their actions on the long run.

A better evaluation of the body’s ability to fight tumours

Some individuals are better able to fight cancer for many years compared with others. This ability to fight tumours depends on the immune response, as observed for colorectal cancers by Jérôme Galon, Research Director at Inserm, and his team, the Laboratory of Integrative Cancer Immunology, at the Cordelier Research Centre (Inserm/UPMC/Paris Descartes University). The investigators show that the proportions of immune system cells in and around the tumour change with the stage of progression of the cancer, and demonstrate the importance of an increased concentration of some cell types to the survival of patients, namely, follicular T-helper cells (Tfh) and B lymphocytes. A better understanding of the dynamics of these cells will help to identify new strategies for developing targeted immunotherapies.

The results of this study are published in the 17 October issue of the journal Immunity.

The immune system is able to fight some tumours before they can affect health. Once the tumour has been identified, immune system cells are mobilised to kill and eliminate the tumour cells. However, tumour cells can sometimes manage to survive the response of the immune cells, and become established. The tumour becomes malignant when it develops in an uncontrolled manner. The investigators at the Cordelier Research Centre (Inserm/UPMC/Paris Descartes University) study the manner in which the immune system fights tumours, in an effort to effectively unleash the body’s intrinsic potential for fighting cancer.

Two factors indicate the body’s potential for “fighting or defeating” a tumour: the intensity of the immune response, and the mechanisms adopted by tumours to escape recognition by the immune system. The complex interactions between tumours and their microenvironment were poorly known until now. In the present study, the investigators examined the spatiotemporal dynamics of 28 different types of immune system cells that infiltrate colorectal tumours. By combining the study of cellular interactions with bioinformatics, they observed that the proportions of immune system cells infiltrating tumours change with the stage of progression of the tumour.

The research team has demonstrated the importance of an increased concentration of some types of immune system cells to patient survival, i.e. the T follicular-helper (Tfh) cells and B lymphocytes. These results obtained for human tumours were also demonstrated in three mouse models of colon cancer.

The investigators also studied more specifically in patients the instability of the gene for the chemokine CXCL13, which modulates the infiltration of Tfh and B lymphocytes. CXCL13 and IL-21 have proven to be additional factors that promote the death of tumour cells: high levels of these molecules are correlated with patient survival.

These observations indicate that T, Tfh and B lymphocytes form a network of cells that communicate inside tumours. High levels of Tfh and B lymphocytes prevent tumour progression and recurrence in colorectal cancer. As in patients, T, Tfh and B lymphocytes control tumour development in murine models of colon cancer.

“The immune response develops during cancer progression. The immune landscape that we describe in relation to colorectal tumours helps us to understand this development in order to intervene in the right place at the right time,” explains Jérôme Galon, Research Director at Inserm and last author of the study. The clinical outcome is highly variable among patients with the same stage cancer. Understanding why some individuals are able to defend themselves against cancer for many years is crucial in combating the disease,” concludes the main author of the study.

The investigators have also developed a test, known as “Immunoscore,” which predicts the ability of an individual’s immune system to fight tumour cells. Using Immunoscore as part of routine prognostic evaluation may provide critical new information on prognosis, and facilitate clinical decision-making (including guidance for therapeutic decisions). In order to promote Immunoscore for routine use in hospitals, an international consortium directed by Jérôme Galon has been launched in association with the US Society for Immunotherapy of Cancer (SITC) and a large number of international institutions from 17 countries throughout the world.

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Large European study finds exposure to even low levels of air pollution during pregnancy increases risk of lower birthweight babies

Exposure to common air pollutants and traffic during pregnancy significantly increases the risk of restricted fetal growth, even at levels well below those stipulated in current European Union (EU) air-quality directives, according to one of the largest cohort studies of its kind published in The Lancet Respiratory Medicine.

The researchers estimate that for every increase of 5 micrograms per cubic meter (5µg/m³) in exposure to fine particulate matter during pregnancy, found in for example traffic fumes and industrial air pollutants, the risk of low birthweight at term rises by 18%. Importantly, this increased risk persists at levels below the existing EU annual air quality limit of 25µg/m³.

« Lower birthweight babies  is associated with health hazards during childhood and adult » explain Rémy Slama, Inserm research director and lead author of the study.“Our findings suggest that a substantial proportion of cases of low birthweight at term could be prevented in Europe if urban air pollution, particularly fine particulate matter, was reduced”*, explains Dr Marie Pedersen from the Centre for Research in Environmental Epidemiology in Barcelona, Spain. 

Pedersen was part of a team of European researchers coordinated by CREAL (Barcelona) and INSERM (Grenoble) to assess the impact of exposure to low levels of air pollution during pregnancy on low birthweight at term (<2500g, after 37 weeks of gestation) which has been linked with respiratory problems in childhood, as well as other diseases later in life. The study also looked at the impact on head circumference because of the potential effect on neurodevelopment. Using data from the European Study of Cohorts for Air Pollution Effects (ESCAPE), the investigators pooled data from 14 cohort studies in 12 European countries involving over 74 000 women who had singleton babies between Feb, 1994 and June, 2011. Air pollution concentrations of nitrogen oxides and particulate matter were estimated at the home addresses using land-use regression models. Traffic density on the nearest road and total traffic load on all major roads within 100m of the residence were also recorded. All air pollutants, particularly fine particulate matter (PM 2.5; with a diameter of 2.5 micrometers or less), and traffic density increased the risk of term low birthweight and reduced average head circumference at birth, after accounting for other factors like maternal smoking, age, weight, and education. Average exposure levels of PM2.5 during pregnancy in the study population ranged from less than 10μg/m³ to nearly 30μg/m³. The researchers estimated that if levels of PM 2.5 were reduced to 10µg/m³ (the WHO annual average air quality guideline value), 22% of cases of low birthweight among term deliveries could be prevented. According to co-author Professor John Wright, director of the Bradford Institute for Health Research in the UK, “The widespread exposure of pregnant women worldwide to urban ambient air pollution at similar or even higher concentrations than those assessed in our study provides a clear message to policy makers to improve the quality of the air we all share.”

Fine-tuning the approach to malaria and toxoplasmosis research

A study carried out by teams from the Institut Pasteur, the Institut Cochin (Inserm, CNRS, Paris Descartes University), and the Wellcome Trust Centre for Molecular Parasitology at the University of Glasgow, may very well redefine current approaches to malaria and toxoplasmosis research in terms of treatment development. Their research which focuses on the role played by the protein AMA1 (present in both parasites) was published october 9, on the Nature Communications website. For many years AMA1 has been the focus of studies aiming to develop malaria treatments and vaccines. However, the authors of this study express their reservations about strategies that focus strictly on blocking AMA1 and show that malaria and toxoplasmosis parasites without AMA1 are still capable of developing normally. 

photo CP toxoplasmose

Stade mérozoïte de Plasmodium falciparum – Copyright Institut Pasteur

One million people die each year from malaria, making it the most widespread parasitic disease in the world today. Toxoplasmosis, which often presents no symptoms in healthy subjects, is a parasitic disease that mainly affects immunedeficient individuals. Pregnant women are also particularly at risk for this disease and if infected for the first time during their pregnancy could spread infection to the fetus.

Plasmodium and Toxoplasma, genera of apicomplexan parasites, are the agents responsible for these diseases. They both contain the same protein, AMA1, which many studies consider necessary for parasites to enter host cells and propagate infection. Because of this, numerous studies conducted since the discovery of the protein have made it their primary focus in the development of anti-parasitic treatments. However, this trend may soon change, thanks to the collaborative efforts of Robert Ménard (Institut Pasteur, Paris), Isabelle Tardieux (Institut Cochin, Paris), Markus Meissner (University of Glasgow), and their teams. These scientists recently showed that in the total absence of AMA1 Plasmodium berghei and Toxoplasma gondii are still capable of entering infected cells and multiplying. This discovery could have a significant impact on how research is conducted in the development of treatments for malaria and toxoplasmosis.

In 2011, the scientists had already shown that parasites genetically modified with very low levels of AMA1 were still able to infect host cells. In today’s study, parasites were created free of all AMA1 using “reverse genetics” (a technique never before used in this field). The scientists showed that in the absence of AMA1, during the blood and hepatic stages of Plasmodium berghei, as well as during the replication stage of Toxoplasma gondii (the stage where the disease spreads to humans), the parasites were still able to enter host cells. What was affected by the lack of AMA1, however, was the parasites’ ability to bind to host cells (this is the step that precedes cell entry). Because of this, the scientists concluded that AMA1 is not a requirement for cell entry but rather is used to bind parasites to the host cells. These observations have prompted the scientists to put forward new recommendations for optimizing research that focuses on AMA1 for the development of new treatments. In particular, they suggest that therapeutic strategies and vaccine development should focus on other proteins in addition to AMA1.

(French) : Fête de la science 2013 : rendez-vous du 17 au 19 octobre 2013 pour « Sciences au Carré(e) »